Résumé
The aim of the present study was to assess the effects of replacing corn silage with sugarcane in the diet of lactating Saanen goats and to determine their intake and digestibility of nutrients, ingestive behavior, milk yield and composition. The experimental diets were composed of increasing levels (0, 33, 66 and 100%) of substitution in dry matter (DM). Twelve multiparous Saanen goats, with an average body weight of 45.2kg, average milk yield of 3.0kg day-1, distributed in a triple latin square experimental design (4 × 4) were used. The dry matter intake (DMI) and other nutrients were estimated through the difference between the total nutrient in the food offered and its total in the leftovers. The DMI, crude protein, neutral detergent fiber (NDF) and total digestible nutrients were not influenced, but the apparent digestibility of DM and NDF decreased. Feeding time and feeding efficiency were not influenced, the rumination and total chewing times increased, and the leisure time decreased, both linearly. Milk yield was not influenced by substitution levels, but corrected milk yield to 3.5% fat decreased. Sugar cane represents a dietary alternative for goats with medium milk yield in critical periods of forage, since it does not change the consumption of DM and milk yield, even with the apparent declining digestibility of some nutrients, influencing the ingestive behavior of the animals.(AU)
O objetivo do presente estudo foi avaliar os efeitos da substituição da silagem de milho por cana-de-açúcar na dieta de cabras Saanen em lactação e determinar a ingestão e a digestibilidade de nutrientes, o comportamento ingestivo, a produção e a composição do leite. As dietas experimentais foram compostas de níveis crescentes (0, 33, 66 e 100%) de substituição na matéria seca (MS). Doze cabras Saanen multíparas, com peso corporal médio de 45,2kg, produção média de leite de 3,0kg dia-1, foram distribuídas em delineamento experimental triplo quadrado latino (4 × 4). A ingestão de matéria seca (IMS) e de outros nutrientes foi estimada por meio da diferença entre o total de nutrientes nos alimentos oferecidos e o total nas sobras. A IMS, a proteína bruta, a fibra em detergente neutro (FDN) e os nutrientes digestíveis totais não foram influenciados, mas a digestibilidade aparente da MS e da FDN diminuiu. A produção de leite não foi influenciada pelos níveis de substituição, mas a produção de leite corrigida para 3,5% de gordura diminuiu. A cana-de-açúcar representa uma alternativa alimentar para cabras com produção média de leite em períodos críticos de forragem, pois não altera o consumo de MS e a produção de leite, mesmo diminuindo a digestibilidade aparente de alguns nutrientes e influenciando o comportamento ingestivo dos animais.(AU)
Sujets)
Animaux , Femelle , Capra/métabolisme , Fibre alimentaire/administration et posologie , Saccharum , Aliment pour animaux , Phénomènes physiologiques de l'appareil digestif , Consommation alimentaireRésumé
Avaliou-se o consumo e digestibilidade dos nutrientes em dietas para cabras da raça Saanen arranjadas em um quadrado latino 5x5, alimentadas com cana-de-açúcar em substituição (0, 25, 50, 75 e 100%) ao feno de capim-tifton 85. O experimento foi constituído de cinco períodos de 15 dias (10 dias para adaptação dos animais às dietas experimentais e 5 dias para coleta de dados e amostras). O consumo voluntário foi calculado pela diferença entre o ofertado e as sobras. Utilizou-se o óxido crômico para estimativa da produção de matéria seca fecal. A digestibilidade aparente da matéria seca, matéria orgânica, extrato etéreo e fibra em detergente neutro foi influenciada negativamente com a substituição, enquanto a digestibilidade da proteína e dos carboidratos não fibrosos não sofreu influência. O baixo consumo de matéria seca de rações com cana-de-açúcar torna-se um fator limitante para cabras de média a alta produção de leite.
The intake and digestibility of nutrients in the diets of Saanen goats arranged in a 5x5 Latin square design, fed with sugar cane replacement (0, 25, 50, 75 and 100%) hay Tifton 85 were evaluated. The experiment consisted of 5 periods of 15 days (10 days for animal adaptation to experimental diets and 5 days for data collection). The voluntary intake was calculated as the difference between the offered and leftovers. Digestibility chromic oxide was used to estimate the fecal dry matter production. The digestibility of dry matter, organic matter, ether extract and neutral detergent fiber was negatively influenced, whereas the digestibility of protein and non-fiber carbohydrates were not affected. The low dry matter intake of diets with sugar cane becomes a limiting factor for goats medium for high milk production.
Sujets)
Animaux , Capra/physiologie , Saccharum/effets indésirables , Aliment pour animaux/analyse , Aliment pour animaux/normesRésumé
Activation of 5-hydroxytryptamine (5-HT) 5-HT1A, 5-HT2C, 5-HT3, and 5-HT7 receptors modulates the excitability of cardiac vagal motoneurones, but the precise role of 5-HT2A/2B receptors in these phenomena is unclear. We report here the effects of intracisternal (ic) administration of selective 5-HT2A/2B antagonists on the vagal bradycardia elicited by activation of the von Bezold-Jarisch reflex with phenylbiguanide. The experiments were performed on urethane-anesthetized male Wistar rats (250-270 g, N = 7-9 per group). The animals were placed in a stereotaxic frame and their atlanto-occipital membrane was exposed to allow ic injections. The rats received atenolol (1 mg/kg, iv) to block the sympathetic component of the reflex bradycardia; 20-min later, the cardiopulmonary reflex was induced with phenylbiguanide (15 µg/kg, iv) injected at 15-min intervals until 3 similar bradycardias were obtained. Ten minutes after the last pre-drug bradycardia, R-96544 (a 5-HT2A antagonist; 0.1 µmol/kg), SB-204741 (a 5-HT2B antagonist; 0.1 µmol/kg) or vehicle was injected ic. The subsequent iv injections of phenylbiguanide were administered 5, 20, 35, and 50 min after the ic injection. The selective 5-HT2A receptor antagonism attenuated the vagal bradycardia and hypotension, with maximal effect at 35 min after the antagonist (pre-drug = -200 ± 11 bpm and -42 ± 3 mmHg; at 35 min = -84 ± 10 bpm and -33 ± 2 mmHg; P < 0.05). Neither the 5-HT2B receptor antagonists nor the vehicle changed the reflex. These data suggest that central 5-HT2A receptors modulate the central pathways of the parasympathetic component of the von Bezold-Jarisch reflex.
Sujets)
Animaux , Mâle , Rats , Bradycardie/physiopathologie , /physiologie , Réflexe/effets des médicaments et des substances chimiques , Nerf vague/effets des médicaments et des substances chimiques , Analgésiques/pharmacologie , Aténolol/pharmacologie , Biguanides/pharmacologie , Bradycardie/induit chimiquement , Rat Wistar , Réflexe/effets des radiations , Agonistes des récepteurs de la sérotonine/pharmacologie , Nerf vague/physiopathologieRésumé
Nitric oxide (NO) influences renal blood flow mainly as a result of neuronal nitric oxide synthase (nNOS). Nevertheless, it is unclear how nNOS expression is modulated by endogenous angiotensin II, an inhibitor of NO function. We tested the hypothesis that the angiotensin II AT1 receptor and oxidative stress mediated by NADPH oxidase contribute to the modulation of renal nNOS expression in two-kidney, one-clip (2K1C) hypertensive rats. Experiments were performed on male Wistar rats (150 to 170 g body weight) divided into 2K1C (N = 19) and sham-operated (N = 19) groups. nNOS expression in kidneys of 2K1C hypertensive rats (N = 9) was compared by Western blotting to that of 2K1C rats treated with low doses of the AT1 antagonist losartan (10 mg·kg-1·day-1; N = 5) or the superoxide scavenger tempol (0.2 mmol·kg-1·day-1; N = 5), which still remain hypertensive. After 28 days, nNOS expression was significantly increased by 1.7-fold in the clipped kidneys of 2K1C rats and by 3-fold in the non-clipped kidneys of 2K1C rats compared with sham rats, but was normalized by losartan. With tempol treatment, nNOS expression increased 2-fold in the clipped kidneys and 1.4-fold in the non-clipped kidneys compared with sham rats. The changes in nNOS expression were not followed by changes in the enzyme activity, as measured indirectly by the cGMP method. In conclusion, AT1 receptors and oxidative stress seem to be primary stimuli for increased nNOS expression, but this up-regulation does not result in higher enzyme activity.
Sujets)
Animaux , Mâle , Rats , Angiotensine-II/physiologie , Hypertension rénovasculaire/enzymologie , NADPH oxidase/effets des médicaments et des substances chimiques , Nitric oxide synthase type I/métabolisme , Stress oxydatif/effets des médicaments et des substances chimiques , Antagonistes du récepteur de type 1 de l'angiotensine-II/pharmacologie , Angiotensine-II/antagonistes et inhibiteurs , N-oxydes cycliques/pharmacologie , Modèles animaux de maladie humaine , Hypertension rénovasculaire/physiopathologie , Losartan/pharmacologie , NADPH oxidase/physiologie , Stress oxydatif/physiologie , Rat Wistar , Marqueurs de spinRésumé
The present study focused on the role of sympathetic renal nerve activity, in mediating congestive heart failure-induced sodium retention following experimental chronic myocardial infarction. Groups of male Wistar rats (240-260 g) were studied: sham-operated coronary ligation (CON3W, N = 11), coronary ligation and sham-operated renal denervation (INF3W, N = 19), 3 weeks of coronary ligation and sympathetic renal nerve denervation (INF3WDX, N = 6), sham-operated coronary ligation (N = 7), and 16 weeks of coronary ligation (INF16W, N = 7). An acute experimental protocol was used in which the volume overload (VO; 5 percent of body weight) was applied for 30 min after the equilibration period of continuous iv infusion of saline. Compared to control levels, VO produced an increase (P < 0.01, ANOVA) in urine flow rate (UFR; 570 percent) and urinary sodium excretion (USE; 1117 percent) in CON3W. VO induced a smaller increase (P < 0.01) in USE (684 percent) in INF3W. A similar response was also observed in INF16W. In INF3WDX, VO produced an immediate and large increase (P < 0.01) in UFR (547 percent) and USE (1211 percent). Similarly, in INF3W VO increased (P < 0.01) UFR (394 percent) and USE (894 percent). Compared with INF3W, VO induced a higher (P < 0.01) USE in INF3WDX, whose values were similar to those for CON3W. These results suggest that renal sympathetic activity may be involved in sodium retention induced by congestive heart failure. This premise is supported by the observation that in bilaterally renal denervated INF3WDX rats myocardial infarction was unable to reduce volume expansion-induced natriuresis. However, the mechanism involved in urinary volume regulation seems to be insensitive to the factors that alter natriuresis.
Sujets)
Animaux , Mâle , Rats , Rein , Infarctus du myocarde , Natriurèse , Système nerveux sympathique , Maladie chronique , Modèles animaux de maladie humaine , Défaillance cardiaque , Hémodynamique , Infarctus du myocarde , Rat WistarRésumé
The two-kidney, one-clip renovascular (2K1C) hypertension model is characterized by a reduction in renal flow on the clipped artery that activates the renin-angiotensin system. Endothelium dysfunction, including diminished nitric oxide production, is also believed to play a role in the pathophysiology of this model. Some studies have shown an effect of L-arginine (L-Arg, a nitric oxide precursor) on hypertension. In the present study we determined the ability of L-Arg (7 days of treatment) to reduce blood pressure and alter renal excretions of water, Na+ and K+ in a model of 2K1C-induced hypertension. Under ether anesthesia, male Wistar rats (150-170 g) had a silver clip (0.20 mm) placed around the left renal artery to produce the 2K1C renovascular hypertension model. In the experimental group, the drinking water was replaced with an L-Arg solution (10 mg/ml; average intake of 300 mg/day) from the 7th to the 14th day after surgery. Sham-operated rats were used as controls. At the end of the treatment period, mean blood pressure was measured in conscious animals. The animals were then killed and the kidneys were removed and weighed. There was a significant reduction of mean blood pressure in the L-Arg-treated group when compared to control (129 ± 7 vs 168 ± 6 mmHg, N = 8-10 per group; P<0.05). Concomitantly, a significant enhancement of water and Na+ excretion was observed in the 2K1C L-Arg-treated group when compared to control (water: 13.0 ± 0.7 vs 9.2 ± 0.5 ml/day, P<0.01; Na+: 1.1 ± 0.05 vs 0.8 ± 0.05 mEq/day, respectively, P<0.01). These results show that orally administered L-Arg acts on the kidney, possibly inducing changes in renal hemodynamics or tubular transport due to an increase in nitric oxide formation
Sujets)
Animaux , Mâle , Rats , Arginine , Pression sanguine , Hypertension rénovasculaire , Sodium , Modèles animaux de maladie humaine , Diurèse , Natriurèse , Rat WistarRésumé
The present study was designed to evaluate the differences in the coronary vasodilator actions of serotonin (5-HT) in isolated heart obtained from naive or castrated male and female rats that were treated with either estrogen or testosterone. Hearts from 12 groups of rats were used: male and female naive animals, castrated, castrated and treated with 17ß-estradiol (0.5 æg kg-1 day-1) for 7 or 30 days, and castrated and treated with testosterone (0.5 mg kg-1 day-1) for 7 or 30 days. After treatment, the vascular reactivity of the coronary bed was evaluated. Baseline coronary perfusion pressure (CPP) was determined and dose-response curves to 5-HT were generated. Baseline CPP differed between male (70 Ý 6 mmHg, N = 10) and female (115 Ý 6 mmHg, N = 12) naive rats. Maximal 5-HT-induced coronary vasodilation was higher (P<0.05) in naive female than in naive male rats. In both sexes, 5-HT produced endothelium-dependent coronary vasodilation. After castration, there was no significant difference in baseline CPP between hearts obtained from male and female rats (75 Ý 7 mmHg, N = 8, and 83 Ý 5 mmHg, N = 8, respectively). Castration reduced the 5-HT-induced maximal vasodilation in female and male rats (P<0.05). Estrogen treatment of castrated female rats restored (P<0.05) the vascular reactivity. In castrated male rats, 30 days of estrogen treatment increased (P<0.05) the responsiveness to 5-HT. The endothelium-dependent coronary vasodilator actions of 5-HT are greater in female rats and are modulated by estrogen. A knowledge of the mechanism of action of estrogen on coronary arteries could aid in the development of new therapeutic strategies and potentially decrease the incidence of cardiovascular disease in both sexes
Sujets)
Animaux , Rats , Mâle , Femelle , Circulation coronarienne/effets des médicaments et des substances chimiques , Piégeurs de radicaux libres/pharmacologie , Hormones sexuelles stéroïdiennes/pharmacologie , Sérotonine/pharmacologie , Vasodilatation/effets des médicaments et des substances chimiques , Castration , Relation dose-effet des médicaments , Oestrogènes/pharmacologie , Perfusion , Rat Wistar , Testostérone/pharmacologie , Résistance vasculaire/effets des médicaments et des substances chimiquesRésumé
The "regional basic diet" or RBD is a multideficient diet (providing 8 percent protein) which is known to produce dietary deficiencies in some populations in northeastern Brazil. The present study investigated the effects of RBD-induced malnutrition on resting blood pressure and baroreflex sensitivity in conscious rats. Malnourished rats were obtained by feeding dams the RBD during mating and pregnancy (RBD-1 group) or during nursing and a 10-day period after weaning (RBD-2 group). At 90 days of age, only RBD-2 rats weighed significantly (P<0.001) less than control rats born to dams fed a standard commercial diet (23 percent protein) during pregnancy and nursing. Baseline mean arterial pressure and heart rate of both RBD-1 and RBD-2 rats were comparable to those of controls. The slopes for both reflex bradycardia and tachycardia (bpm/mmHg) induced by intravenous phenylephrine and sodium nitroprusside, respectively, were unchanged in either RBD-1 (-2.08 0.11 and -3.10 0.43, respectively) or RBD-2 (-2.32 0.30 and -3.73 0.53, respectively) rats, when compared to controls (-2.09 0.10 and -3.17 0.33, respectively). This study shows that, after a prolonged period of nutritional recovery, the patterns of resting blood pressure and baroreflex sensitivity of both pre- and postnatally malnourished rats were similar to those of controls. The decreased body weight and the tendency to increased reflex tachycardia in RBD-2 rats may suggest that this type of maternal malnutrition during lactation is more critical than during pregnancy
Sujets)
Animaux , Mâle , Femelle , Rats , Grossesse , Baroréflexe , Pression sanguine , Régime alimentaire/effets indésirables , Malnutrition protéinocalorique/étiologie , Analyse de variance , Poids de naissance , Brésil , Études cas-témoins , Sédation consciente , Rythme cardiaque , Malnutrition protéinocalorique/complications , Rat Wistar , Tachycardie/étiologieRésumé
Cardiopulmonary reflexes are activated via changes in cardiac filling pressure (volume-sensitive reflex) and chemical stimulation (chemosensitive reflex). The sensitivity of the cardiopulmonary reflexes to these stimuli is impaired in the spontaneously hypertensive rat (SHR) and other models of hypertension and is thought to be associated with cardiac hypertrophy. The present study investigated whether the sensitivity of the cardiopulmonary reflexes in SHR is restored when cardiac hypertrophy and hypertension are reduced by enalapril treatment. Untreated SHR and WKY rats were fed a normal diet. Another groups of rats were treated with enalapril (10 mg kg-1 day-1, mixed in the diet; SHRE or WKYE) for one month. After treatment, the volume-sensitive reflex was evaluated in each group by determining the decrease in magnitude of the efferent renal sympathetic nerve activity (RSNA) produced by acute isotonic saline volume expansion. Chemoreflex sensitivity was evaluated by examining the bradycardia response elicited by phenyldiguanide administration. Cardiac hypertrophy was determined from the left ventricular/body weight (LV/BW) ratio. Volume expansion produced an attenuated renal sympathoinhibitory response in SHR as compared to WKY rats. As compared to the levels observed in normotensive WKY rats, however, enalapril treatment restored the volume expansion-induced decrease in RSNA in SHRE. SHR with established hypertension had a higher LV/BW ratio (45 percent) as compared to normotensive WKY rats. With enalapril treatment, the LV/BW ratio was reduced to 19 percent in SHRE. Finally, the reflex-induced bradycardia response produced by phenyldiguanide was significantly attenuated in SHR compared to WKY rats. Unlike the effects on the volume reflex, the sensitivity of the cardiac chemosensitive reflex to phenyldiguanide was not restored by enalapril treatment in SHRE. Taken together, these results indicate that the impairment of the volume-sensitive, but not the chemosensitive, reflex can be restored by treatment of SHR with enalapril. It is possible that by augmenting the gain of the volume-sensitive reflex control of RSNA, enalapril contributed to the reversal of cardiac hypertrophy and normalization of arterial blood pressure in SHR.
Sujets)
Animaux , Mâle , Rats , Antihypertenseurs/usage thérapeutique , Énalapril/usage thérapeutique , Hypertension artérielle/traitement médicamenteux , Hypertrophie ventriculaire gauche/traitement médicamenteux , Réflexe/physiologie , Antihypertenseurs/toxicité , Pression sanguine/effets des médicaments et des substances chimiques , Énalapril/toxicité , Coeur/physiologie , Hypertension artérielle/physiopathologie , Hypertrophie ventriculaire gauche/physiopathologie , Poumon/physiologie , Rat WistarRésumé
Cardiac hypertrophy that accompanies hypertension seems to be a phenomenon of multifactorial origin whose development does not seem to depend on an increased pressure load alone, but also on local growth factores and cardioadrenergic activity. The aim of the present study was to determine if sympathetic renal denervation and its effects on arterial pressure level can prevent cardiac hypertrophy and if it can also delay the onset and attenuate the severity of deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt treatment was initiated in rats seven days after uninephrectomy and contralateral renal denervation or sham renal denervation. DOCA (15 mg/kg, sc) or vehicle (soybean oil, 0.25 ml per animal) was administered twice a week for two weeks. Rats treated with DOCA or vehicle (control) were provided drinking water containing 1 percent NaCl and 0.03 percent KCl. At the end of the treatment period, mean arterial pressure (MAP) and heart rate measurements were made in conscious animals. Under ether anesthesia, the heart was removed and the right and left ventricles (including the septum) were separated and weighed. DOCA-salt treatment produced a significant increase in left ventricular weight/body weight (LVW/BW) ratio (2.44 + 0.09 mg/g) and right ventricular weight/body weight (RVW/BW) ratio (0.53 + 0.01 mg/g) compared to control (1.92 + 0.04 and 0.48 + 0.01 mg/g, respectively) rats. MAP was significantly higher (39 percent) in DOCA-salt rats. Renal denervation prevented (P>0.05) the development of hypertension in DOCA-salt rats but did not prevent the increase in LVW/BW (2.27 + 0.03 mg/g) and RVW/BW (0.52 + 0.01 mg/g). We have shown that the increase in arterial pressure level is not responsible for cardiac hypertrophy, which may be more related to other events associated with DOCA-salt hypertension, such as an increase in cardiac sympathetic activity.
Sujets)
Rats , Animaux , Mâle , Pression sanguine/effets des médicaments et des substances chimiques , Cardiomégalie , Désoxycorticostérone/usage thérapeutique , Rein/innervation , Rein/chirurgie , Chlorure de sodium alimentaire , Cardiomégalie/traitement médicamenteux , Cardiomégalie/étiologie , Rythme cardiaque/effets des médicaments et des substances chimiques , Taille d'organe , Rat WistarRésumé
The maintenance of arterial pressure at levels adequate to perfuse the tissues is a basic requirement for the constancy of the internal environment and survival.The objective of the present review was to provide information about the basic relfex mechanisms that are responsible for the moment-to-moment regulation of the cardiovascular system. We demonstrate that this control is largely provided by the action of arterial and non-arterial reflexes that detect and correct changes in arterial pressure (baroreflex), blood volume or chemical composition (mechano-and chemosensitive cardiopulmonary reflexes), and changes in bloodgas composition (chemoreceptor reflex). The importance of the integration of these cardiovascular reflexes is well understood and it is clear that processing mainly occurs in the nucleus tractus solitarii, although the mechanism is poorly understood.There are several indications that the interactions of baroreflex, chemoreflex and Bezold-Jarisch reflex inputs, and the central nervous system control the activity of autonomic preganglionic neurons through parallel afferent and efferent pathways to achieve cardiovascular homeostasis. It is surprising that so little appears in the literature about the integration of these neural reflexes in cardiovascular function. Thus, our purpose was to review the interplay between peripheral neural reflex mechanisms of arterial blood pressure and blood volume regulation in physiological and pathophysiological states. Special emphasis is placed on the experimental model or arterial hypertension induced by N-nitro-L-arginine methyl ester (L-NAME) in which the interplay of these three reflexes is demonstrable.
Sujets)
Lapins , Rats , Animaux , Baroréflexe/physiologie , Pression sanguine/physiologie , Cellules chimioréceptrices/physiopathologie , Cystéine/pharmacologie , Hypertension artérielle/physiopathologie , Infarctus du myocarde/physiopathologie , Cyanure de potassium/pharmacologie , Barorécepteurs/physiopathologie , Sérotonine/pharmacologie , Cellules chimioréceptrices/effets des médicaments et des substances chimiques , Hypertension artérielle/traitement médicamenteux , Anatomopathologie , Barorécepteurs/effets des médicaments et des substances chimiquesRésumé
We have reported that chlorthalidone (Chlor) prevents the development of heart hypertrophy in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The present study was carried out to determine whether Chlor (8 mg/day per animal, added to the food, for 20 days) affects kidney and heart hypertrophy in DOCA-salt (8 mg/kg, sc, twice a week) rats by causing alterations in protein and peptide hydrolysis Heart (left ventricle) and kidney enzyme activities were measured i tissue homogenates from normal-control, salt-control, DOCA-sa salt and DOCA-salt-Chlor male Wistar rats (N = 6 for each group), using azocasein as the substrate for proteolytic enzymes and specific peptides for prolylendopeptidase (PEP) and multicatalytic proteinase (MCP). The tissue weight/body weight ratio increased in parallel to elevation of blood pressure. The left ventricular muscle hypertrophy (26 per cent, P<0.05) present in the DOCA-salt hypertensive group was completely prevented by simultaneous Chlor treatment. Chlor treatment did not change the kidney hypertrophy (+79 per cent, P<0.05) observe in the salt-control (+57 per cent, P<0.05) and DOCA-salt (+74 per cent, P<0.05) groups. The hydrolysis of peptides by PEP and MCP was similar in the normal and salt-control groups. The heart PEP activity was 24 per cent higher (P<0.01) in DOCA-salt rats, whereas MCP activity was not different when compared to control groups. DOCA-salt treatment increased MCP activity in the kidney by 44 per cent while PEP activity did not differ from that of control groups. The hydrolysis of proteins by heart enzymes was increased by salt by 47 per cent. Chlor treatment restored the reduction in protein hydrolysis induced by DOCA-salt (a 21 per cent decrease, P<0.05) to a level similar to that of the normal-control group. Similarly, Chlor coadministration prevented the 30 per cent reduction in renal proteolytic activity elicited by DOCA-salt treatment. Although Chlor treatment prevented the DOCA-salt-induced reduction in protein hydrolysis, this response did not interfere with kidney hypertrophy. The mechanism by which hypertension produces hypertrophy is unclear, but our results suggest that this structural modification is not related to the activities of some peptidases, e.g. protein and peptide hydrolases.
Sujets)
Rats , Animaux , Mâle , Chlortalidone/usage thérapeutique , Désoxycorticostérone/administration et posologie , Hypertension artérielle/thérapie , Peptide hydrolases/composition chimique , Hypertension artérielle/induit chimiquement , Rat WistarRésumé
The present study was designed investigate the role of cardio-pulmonary reflex, more specifically the bezold-Jarisch reflex, in experimental hypertension induced by chronic administration of Nw-nitro-L-arginine methyl ester (L-NAME) (0,5 mg/ml) added to the drinking water for 6 days. The study was perfomed in male Wistar rats (200-350 g), 9 animals per group. L-NAME ingestion caused a significant increase in resting mean arterial pressure (MAP: 182 + or - 4mmHg) and heart rate (HR: 447 = or - 20 bpm) when compared to untreated rats (MAP: 112 = or - 3 mmHg and HR: 355 + or - 10 bpm). Cardiopulmonary receptors were chemically stimulated with bolus injections of 5-hydroxytryptamine (5-HT, 4-10 ug/Kg, iv) followed by measuring the falls in diastolic arterial pressure (DAP) and HR in conscious and freely moving animals. An expected, the responses to intravenous injections of 5-HT consisted of a dose-dependent reduction in HR (from 26 = or - 14 to 175 + or - 25 bpm) and DAP (from 7 + or - 4 to 39 + or - 3 mmHg) in the control rats. Both bradycardia and diastolic hypotension were significantly accentuated in the L-NAME animals (approximately 30 per cent). These data suggest that, in contrast to other models of hypertension, in the present one caused by inhibition of nitric oxide synthesis, the Bezold-Jarisch reflex exaggerated. This neural dysfunction could be related to changes in the cardiac vagal effrent or effector
Sujets)
Animaux , Rats , Arginine/administration et posologie , Arginine/analyse , Rythme cardiaque , Hypertension artérielle/induit chimiquement , Monoxyde d'azote/antagonistes et inhibiteurs , Pression artérielle , Réflexe/effets des médicaments et des substances chimiques , Arginine/pharmacologie , Monoxyde d'azote/biosynthèse , Rat Wistar , Sérotonine/administration et posologie , VasoconstrictionRésumé
Heart tissue contains large amounts of the Ca²+ -activated protein-ase calpain which has been assigned a specific function in the turnover of muscle protein. The objective of the present study was to determine calpain (E.C. 3.4.22.17)-like activity in homogenates of left ventricle from hypertensive rats that developed ventricular hypertrophy. Calpain activity was assayed using heat-denaturated azocasein as a substrate in the presence of 1 mM calcium and corrected by subtraction of the Ca²+ -independent activities. Tha latter were measured in the presence of 1 mM EGTA and the products read at 440nm. Male Wistar rats (225g) were assgned to control (N=8, normal drinking water), salt (N=6, drinking water containing 1 percent NaCl) and DOCA-salt (N=6, deoxycorticosterone acetate, 8 mg/Kg, sc, twice a week for 20 days plus drinking water containing 1 percent NaCl) groups. SHR (N =6, spontaneously hypertensive rats) were also used. The calpain activity of the control group was at 3.90 ñ 0.22 mU/g wet weight tissue. Hypertension induced significant left ventricular hypertrophy in DOCA-salt rats (26 percent) and in SHR (54 percent) and a 30 percent decrease in calpain activity in both groups (P < 0.01). In the high salt load (salt group) calpain activity was also decreased, but this was not accompanied by hypertrophy...
Sujets)
Animaux , Mâle , Rats , Calpain/métabolisme , Désoxycorticostérone/administration et posologie , Hypertrophie ventriculaire gauche/physiopathologie , Dénaturation des protéines , Rats de lignée SHR , Rat Wistar , Extraits tissulaires/physiologieRésumé
1. Heart mass, prolyl endopeptidase activity and fractionated proteins from heart tissue were studied in one-kidney, one clip hypertensive rats (N=6) and compared to sham-operated rats (N=6). 2. Body weigh, arterial pressure and tissue mass were measured 4 weeks after artery clipping Z-Gly-Pro-p-nitroaniline hydrolysis was used to measure tissue prolyl endopeptidase activity in the homogenate. Protein was fractionated into the soluble and myofibrillar fractions. 3. In the normotensive rats, prolyl endopeptidase activity expressed in terms of protein specific activity (µM substrate hydrolyzed h-1 mg supernatant protein-1) occurred in atria and was 2.5-fold higher than in the ventricles (3.79 ñ 0.20 vs 1.44 ñ 0.02, P<0.05). In the one-kidney, one clip hypertensive rats, the left ventricle tissue increased 1.7-fold (2.27 ñ 0.11 vs 3.72 ñ 0.11 mg wet weight tissue/g body weight, P<0.001), the soluble protein fraction (54.86 ñ 3.60 vs 57.38 ñ 6.64 mg/g wet weight tissue) was unchanged, while the myofibrillar fraction increased 1.9-fold (118.9 ñ 9.09 vs 229.8 ñ 8.47 mg/g wet weight tissue, P<0.001). 4 The specific activity of the atrial and ventricular prolyl endopeptidase decreased in atria and increased in ventricles as the result of hypertension (3.79 ñ 0.2 vs 2.84 ñ 0.13 and 1.44 ñ 0.02 vs 1.87 ñ 0.13; respectively). These regional differences in prolyl endopeptidase enxyme content caused by one-kidney, one clip hypertension in neurosecretory and non-neurosecretory heart areas suggest that this enzyme plays a local role in the turnover of specific polypeptides
Sujets)
Animaux , Mâle , Rats , Hypertension rénovasculaire/enzymologie , Myocarde/enzymologie , Protéases à sérine/métabolisme , Analyse de variance , Rat WistarRésumé
The time course of changes in baroreceptor reflex sensitivity in Goldblatt two-kidney one clip (2K1C) hypertension was studied 3, 7 and 30 days after renal artery clipping by means of a sigmoidal curve-fitting analysis. Experiments were performed in 54 adult male Wistar rats (N = 9 per group) weighing 200-300 g. The reflex heart rate responses were elicited by alternate intravenous bolus injections of phenylephrine (delta +5 to +50 mmHg) and sodium nitroprusside (delta -5 to -50 mmHg). A clear upper and lower plateau (reflex tachycardia and bradycardia, respectively) was noted in both sham and hypertensive groups. Although the resting mean arterial pressure was significantly increased in all hypertensive groups (131 +/- 3, 149 +/- 7 and 168 +/- 11 mmHg, respectively, 3, 7 and 30 days after clipping), when compared to the sham group (108 +/- 2 mmHg), significant changes in baroreceptor reflex function were observed only in 7- and 30-day groups. Baroreflex sensitivity was markedly reduced in these hypertensive rats (2.3 +/- 0.3 and 1.9 +/- 0.3 bpm/mmHg, respectively) compared to the sham group (4.2 +/- 0.3 bpm/mmHg). In addition, a reduced baroreflex heart rate range was observed in these groups (117 +/- 12 and 107 +/- 10 bpm, respectively) compared to the sham group (165 +/- 11 bpm). These data indicate an impairment of baroreflex function in conscious 2K1C hypertensive rats which seems to be secondary to arterial hypertension.
Sujets)
Animaux , Mâle , Rats , Rythme cardiaque , Hypertension rénovasculaire/physiopathologie , Barorécepteurs , Analyse de variance , Rythme cardiaque/effets des médicaments et des substances chimiques , Modèles logistiques , Nitroprussiate , Phényléphrine , Barorécepteurs , Rat Wistar , Facteurs tempsRésumé
The aim of the present investigation was to study the Bezold-Jarisch reflex in catecholamine-induced myocardial hypertrophy. Ten conscious male albino rats (260-300 g) were treated for 15 days with isoproterenol (IR), 0.3 mg/kg injected im once a day, and compared to 10 control rats (CR) similarly injected with vehicle (0.25 ml). No significant changes in body weight, resting mean arterial pressure or heart rate were observed in the IR group. Left and right ventricular hypertrophy was observed in IR animals (27 and 28, respectively, P < 0.01) when compared to CR. The Bezold-Jarisch reflex was tested by injecting 5-hydroxytryptamine (4-32 micrograms/kg, iv) and was characterized by a simultaneous fall in diastolic arterial pressure (for example: 91 +/- 4 to 61 +/- 3 mm Hg, 16 micrograms/kg) and bradycardia (for example: 330 +/- 10 to 177 +/- 25 bpm, 16 micrograms/kg). This reflex was significantly attenuated in the IR when compared to the CR group. Our data suggest that ventricular hypertrophy without changes in arterial pressure can lead to a reduction of the Bezold-Jarisch reflex. The results reported here are in agreement with other studies showing that the impairment of cardiopulmonary reflex in hypertensive animals and humans occurs exclusively when the hypertension is accompanied by ventricular hypertrophy.
Sujets)
Animaux , Mâle , Rats , Baroréflexe , Cardiomégalie , Baroréflexe , Poids , Cardiomégalie , Rythme cardiaque/effets des médicaments et des substances chimiques , Isoprénaline , Taille d'organe , Pression artérielle/effets des médicaments et des substances chimiques , Repos , Sérotonine , Facteurs tempsRésumé
1. The chronic inhibition of nitric oxide synthesis by N omega-nitro-L-arginine-methyl ester (L-NAME) leads to arterial hypertension accompanied by a significant increase in cardiac sympathetic tone and an almost complete abolition of the vagal tone in conscious adult male Wistar rats. The main aim of the present study was to examine the baroreceptor heart rate reflex function in L-NAME-treated rats (N = 10). 2. Spontaneous daily oral intake of L-NAME (1 mg/ml for 6 days) caused marked hypertension and tachycardia (176 +/- 5 mmHg and 418 +/- 16 bpm), when compared to untreated rats (111 +/- 2 mmHg and 354 +/- 8 bpm). 3. Baroreflex gain was determined in conscious freely moving rats by sigmoidal curve fitting analysis using alternate intravenous injections of phenylephrine (0.2-10.0 micrograms/kg) and sodium nitroprusside (0.5-20.0 micrograms/kg) to produce pressor-induced bradycardia and depressor-induced tachycardia, respectively. The baroreflex gain (sensitivity) was significantly enhanced in L-NAME-treated rats compared to control rats (10.9 +/- 2.5 vs 4.5 +/- 0.3 bpm/mmHg, respectively) mainly due to exaggerated reflex bradycardia responses to increases in arterial hypertension. 4. The data indicate that chronic inhibition of nitric oxide synthesis enhances the bradycardic component of the baroreflex function
Sujets)
Animaux , Mâle , Rats , Baroréflexe/physiologie , Rythme cardiaque/physiologie , Monoxyde d'azote/antagonistes et inhibiteurs , Arginine/administration et posologie , Arginine/analogues et dérivés , Arginine/pharmacologie , Baroréflexe/effets des médicaments et des substances chimiques , Bradycardie/physiopathologie , Rythme cardiaque , Hypertension artérielle/physiopathologie , Injections veineuses , Nitroprussiate/administration et posologie , Monoxyde d'azote/biosynthèse , Phényléphrine/administration et posologie , Pression artérielle , Rat Wistar , Tachycardie/physiopathologie , Facteurs tempsRésumé
The cardiovascular effect of of isoproterenol pretreatment (ISO) mimicking short duration sympathetic hyperacitivity was studied in conscious adult male albino rats. Cardiac hypertrophy of right and left ventricles was observed after pretreatmewnt with isoproterenol for 3 days (0.1 mg/kg, 3 times a day). when compared to saline-treated rats. The pressor response to noradrenaline (NOR, 1 to 1000 ug/kg, iv) was slightly but consistently larger in the ISO group than in the control group (in mm Hg, Control = 109 ñ 3.5; NOR 1 = 114 ñ 3.3; NOR 10=116 ñ 4: NOR 100 = 127 ñ 5.6 and NOR 1000 = 152 ñ 7.3 for saline-treated rats and, Control = 106 ñ 5.1; NOR 1 = 112 ñ 5.1; NOR 10 = 118 ñ 5.3; NOR 100 = 134 ñ 4.9 and NOR 1000 = 162 ñ 7.5 for ISO groups). An increased reflex bradycardia was also observed in response to increasing doses of noradrenaline (in bpm, Control = 323 ñ 5.6; NOR 1 = 313 ñ 6.8; NOR 10 = 309 ñ 8.6; NOR 100 = 293 ñ 7.5 and NOR 1000 = 284 ñ 5.3 for saline-treated rats and Control = 316 ñ 4.3; NOR 10 = 289 ñ 3.4; NOR 100 = 267 ñ 4 and nor 1000 = 251 ñ 2.6 for ISO groups; ANOVA, P<0.01). There were no significant differences autonomic tone to the heart between control and isoproterenol-pretreated animals. The present results indicate that isoproterenol treatment induces significant in vivo cardiovascular modifications
Sujets)
Rats , Cardiomégalie , Coeur/induit chimiquement , Isoprénaline/thérapie , Norépinéphrine/administration et posologieRésumé
We had previously reported that sinoaortic denervation induces cardiac ventricular hypertrophy in rats. The objective of the present study was to determine whether this cardiac hypertrophy can be prevented by inhibition of angiotensin converting enzyme (ACE) with captopril, 20 mg/kg, administered sc twice daily for 15 days. The left ventricular weight/body weight ratio significantly increased (12%) in sinoaortic denervated (SAD) rats 15 days after surgery when compared with the sham-operated group (SO). Administration of captopril to SAD rats prevented this ventricular hypertrophy and decreased but did not completed abolish their high arerial pressure. No changes in the normal pattern of baroreceptor reflex activity were observed in the captopril-pretreated SAD or SO groups. These data suggest the participation of the angiotensin system in the development of cardiac hypertrophy in SAD rats