Controle neurovascular de corredores amadores hipertensos / Neurovascular control of hypertensive amateur runners

INTRODUÇÃO: Alterações neurovasculares presentes na hipertensão arterial são minimizadas pelo treinamento físico em hipertensos previamente sedentários. Entretanto, é desconhecido se atletas hipertensos apresentam alterações neurovasculares ou se o treinamento físico previne tais danos. Este estudo avaliou o controle neurovascular de corredores hipertensos, durante o treinamento competitivo, assim como o efeito de 4 meses de treinamento de intensidade moderada nesta população. MÉTODOS: 37 corredores, homens (20 normotensos, 43 +-1 anos e 17 hipertensos, 42+-1 anos), foram avaliados no treinamento competitivo e posteriormente divididos em 4 subgrupos: normotensos que mantiveram treinamento competitivo (n=10); normotensos que realizaram treinamento de intensidade moderada (n=10); hipertensos que mantiveram treinamento competitivo (n=8); hipertensos que realizaram treinamento de intensidade moderada (n=8). Após 4 meses de intervenção, todos os corredores foram novamente avaliados. Atividade nervosa simpática muscular (ANSM) (microneurografia), propriedades arteriais (velocidade da onda de pulso (VOP) e sistema echo-tracking de alta resolução), controle barorreflexo da frequência cardíaca (FC) e da ANSM (infusão de drogas vasoativas) foram avaliados. RESULTADOS: Corredores hipertensos apresentaram maior pressão arterial sistólica (P < 0,001), diastólica (PAD) (P < 0,001) e média (PAM) (P < 0,001) que corredores normotensos. A ANSM foi maior no grupo hipertenso (disparos/min.; P=0,02 e disparos/100 batimentos; P=0,004) em relação ao grupo normotenso. Não houve diferença na VOP (P=0,71) e nas variáveis da carótida: espessura intima-média (P=0,18), diâmetro (P=0,09) e distensão (P=0,79) entre os grupos. A equação sigmoidal para controle barorreflexo da FC, mostrou menor ganho barorreflexo nos corredores hipertensos em relação aos normotensos (resetting) (P=0,002). O controle barorreflexo da FC, avaliado pela análise de regressão linear, não foi...

INTRODUCTION: Neurovascular alterations presented in hypertension are minimized by physical training in previously sedentary hypertensive. However it is unknown if hypertensive athletes present neurovascular alterations or if physical training prevents these damages. This study evaluated the neurovascular control of hypertensive runners during competitive training as well as the effect of 4 months of moderate intensity training in this population. METHODS: 37 runners, male (20 normotensive, 43+-1 years old and 17 hypertensive, 42+-1 years old), were evaluated during competitive training and after that were divided in 4 subgroups: normotensive who maintained competitive training (n=10); normotensive who performed moderate intensity training (n=10); hypertensive who maintained competitive training (n=8); hypertensive who performed moderate intensity training (n=8). After 4 months of intervention, all the runners were evaluated again. Muscle sympathetic nerve activity (MSNA) (microneurography), arterial properties (pulse wave velocity (PWV) and high-resolution echo-tracking system), baroreflex control of heart rate (HR) and MSNA (infusion of vasoactive drugs) were evaluated. RESULTS: Hypertensive runners had higher systolic (P < 0.001), diastolic (DAP) (P < 0.001) and mean (MAP) (P < 0.001) arterial pressure than normotensive runners. MSNA was higher in hypertensive group (bursts/min.; P=0.02 and bursts/100 heart beats; P=0.004) than in normotensive group. There was no difference in PWV (P=0.71) and carotid variables: intima-media thickness (P=0.18), diameter (P=0.09) and distension (P=0.79) between groups. The gain of baroreflex control of HR, evaluated by sigmoidal logistic equation was lower in hypertensive runners than normotensive runners (resetting) (P=0.002). Baroreflex controf of HR, evaluated by linear equation analysis, was not different between groups during increase (slope P=0.41; intercept P=0.31) and decrease (slope P=0.16...

Efeito da terapêutica com beta-bloqueador na resposta dos quimiorreflexos e ergorreflexo em pacientes com insuficiência cardíaca / Effect of beta-blocker therapeutics on the chemoreflex and ergoreflex response in heart failure patients

A intolerância ao exercício físico na insuficiência cardíaca (IC) está relacionada a alterações hemodinâmicas e neurohumorais pela complexa interação dos reflexos cardiovasculares. Os quimiorreflexos central e periférico e o ergorreflexo estão envolvidos na hiperventilação de repouso e durante o exercício, contribuindo para intolerância ao esforço. Os objetivos do estudo foram avaliar o efeito da terapêutica com beta-bloqueador (betab) na resposta dos quimiorreflexos central e periférico e do ergorreflexo por meio das alterações da resposta ventilatória durante o teste de caminhada de seis minutos (T6M); e avaliar o efeito da sua otimização também sobre as catecolaminas plasmáticas e peptídeo natriurético do tipo B (BNP). Foram estudados 15 pacientes masculinos, 49.5 ± 2.5 anos, com diagnóstico de IC há mais de 3 meses, sem histórico de tratamento com betab, com fração de ejeção (FEVE) 25.9 ± 2.5%, classe funcional I-III (NYHA). Estes pacientes poderiam estar em uso de inibidores da enzima conversora da angiotensina, bloqueadores do receptor da angiotensina II e antagonista do receptor da aldosterona. Todos os indivíduos realizaram testes: ergoespirométrico em esteira segundo o protocolo de Naughton, três T6M em esteira com controle de velocidade pelo paciente randomizados (um com sensibilização dos quimiorreceptores centrais, um com sensibilização dos quimiorreceptores periféricos e um controle em ar ambiente - AA). Também realizaram T6M com e sem oclusão circulatória regional em membro inferior. Em relação aos exames laboratoriais, foram feitas análises de catecolaminas plasmáticas em repouso e BNP. Os pacientes foram então submetidos a tratamento medicamentoso padrão da Instituição, com introdução e otimização da terapêutica com ßb e, após seis meses, foram reavaliados. Após otimização do betab, houve melhora significativa na FEVE, de 26 ± 2,5 para 33 ± 2,6 (p < 0,05); diminuição de níveis de BNP (775 ± 163 para 257 ± 75; p < 0,01) e...

In heart failure (HF), exercise intolerance is related to hemodynamic and neurohumoral alterations by the complex interaction of cardiovascular reflexes. The central and peripheral chemoreflex and the ergoreflex are involved in hyperventilation at rest and during exercise, contributing to exercise intolerance. The aims of the study were to assess the effect of beta-blocker (betab) therapy on the central and peripheral chemoreflexes and ergoreflex responses through ventilatory changes during the six-minute walk test (6MWT), and to assess the effect of betab optimized therapy on plasma catecholamines and B-type natriuretic peptide (BNP). We studied 15 male patients, 49.5 ± 2.5 years, diagnosed with HF for more than three months, never-treated with ßb, ejection fraction (LVEF) 25.9 ± 2.5%, functional class I-III (NYHA). These patients could be in use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and aldosterone antagonists. All subjects underwent the following tests: cardiopulmonary exercise treadmill test according to the Naughton protocol, three randomized treadmill 6MWT with speed controlled by the patient (one with sensitization of central chemoreceptors, one with an awareness of peripheral chemoreceptors and another control in ambiental air - AA). Also all subjects underwent 6MWT with and without regional circulatory occlusion on the lower limb. Regarding laboratory tests, plasma catecholamines concentration at rest and BNP were also analyzed. Patients were then submitted to the institution standard drug therapy, with introduction and optimization of betab and were reassessed six months later. After optimization, there was a significant improvement in LVEF from 26 ± 2.5 to 33 ± 2.6 (p < 0.05); and a decrease in BNP levels (775 ± 163 to 257 ± 75, p < 0.01) and plasma catecholamines (598 ± 104 to 343 ± 40, p < 0.05). There was also a significant decrease in resting heart rate from 95.6 ± 4.5 to 69.0 ± 1.6...

Hipertensión arterial resistente: [revisión] / Resistant hypertension: [review]

Resistant hypertension, defined as a persistent blood pressure over 140/90 mmHg despite the use of three antihypertensive drugs including a diuretic, is unusual. The diagnosis requires ruling out initially pseudoresistance and a lack of compliance with treatment. Ambulatory blood pressure recording allow the recognition of white coat hypertension. When there is a clinical or laboratory suspicion, secondary causes of hypertension should be discarded. Excessive salt intake, the presence of concomitant diseases such as diabetes mellitus, chronic renal disease, obesity, and psychiatric conditions such as panic attacks, anxiety and depression, should also be sought. The presence of target organ damage requires a more aggressive treatment of hypertension. Recent clinical studies indicate that the administration of aldosterone antagonists as a fourth therapeutic line provides significant additional blood pressure reduction, when added to previous antihypertensive regimens in subjects with resistant hypertension. The possible blood pressure lowering effects of prolonged electrical activation of carotid baroreceptors is under investigation.

Does acute hyperglycemia alter rat aortic depressor nerve function?

Because it is not known where in the reflex arch, i.e., afference, central nervous system or efferences, hyperglycemia affects baroreflex function, the present study examined the effect of short-term (30 min) hyperglycemia on aortic depressor nerve function measured by a mean arterial pressure vs aortic depressor nerve activity curve, fitted by sigmoidal regression, or by cross-spectral analysis between mean arterial pressure and aortic depressor nerve activity. Anesthetized male Wistar rats received an intravenous bolus (0.25 mL) injection, followed by 30 min of infusion (1 mL/h) of 30 percent glucose (N = 14). Control groups received a bolus injection and infusion of 0.9 percent saline (N = 14), or 30 percent mannitol (N = 14). Glucose significantly increased both blood glucose and plasma osmolarity (P < 0.05). Mean arterial pressure did not change after glucose, saline or mannitol infusion. Mean arterial pressure vs nerve activity curves were identical before and 10 and 30 min after the beginning of glucose, saline or mannitol infusion. Slow (0.3 Hz) oscillations of arterial pressure were induced by controlled bleeding, and cross-spectral analysis was applied to arterial pressure and aortic nerve activity. Transfer function magnitude (aortic depressor nerve activity/mean arterial pressure ratio in the frequency domain) was calculated as an index of gain of the aortic depressor nerve. Transfer function magnitude was similar in all groups during induced or spontaneous oscillations of arterial pressure. In conclusion, the present study demonstrates, by means of two different approaches for assessing baroreceptor function, that aortic depressor nerve activity was not altered by short-term (30 min) hyperglycemia.

Resveratrol inhibits carotid sinus baroreceptor reflex in anesthetized rats / 中国药理学与毒理学杂志

AIM To study the relationship between cardioprotective effects of resveratrol and carotid sinus baroreflex (CSB). METHODS The functional curve of the CSB was measured by recording changes in arterial pressure in anesthetized male rats with perfused isolated carotid sinus. RESULTS Resveratrol (30, 60 and 120 μmol·L-1) inhibited the CSB, which shifted the functional curve of the baroreflex to the right and upward. There were a marked decrease in peak slope and a reflex decrease of blood pressure, and also an increase in threshold pressure. Changes of these parameters showed a concentration-dependent manner. Pretreatment with Nω-nitro-L-arginine methylester (100 μmol·L-1), an inhibitor of nitric oxide synthase, and pretreatment with Bay K8644 (500 nmol·L-1), an agonist of L-type calcium channel, could both eliminate the inhibitory effect of resveratrol on CSB. A potent inhibitor of tyrosine phosphatase sodium orthovanadate (1 mmol·L-1) did not influence the effect of resveratrol on CSB. CONCLUSION Resveratrol inhibits carotid baroreflex, which may be mediated by the locally released NO and decreased calcium influx.

Inhibitory effect of cholecystokinin octapeptide on carotid sinus nerve afferent discharge in anesthetized rats / 中国药理学与毒理学杂志

AIM To study if cholecystokinin octapeptide (CCK-8) alter cardiovascular functions by its direct inhibitory effect on carotid sinus baroreceptor (CSB) activity. METHODS The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. RESULTS ① CCK-8 0.1, 0.5 and 1.0 μmol·L-1 shifted FCCB to the right and downward, with a marked decrease in peak slope and peak integral value of carotid sinus nerve discharge in a concentration-dependent manner, indicating the inhibitory effect of CCK-8 on CSB activity. ② Pretreatment with proglumide (100 μmol·L-1), a nonselective CCK receptor antagonist, or Bay K8644 (0.5 μmol·L-1), an agonist of calcium channel, partially attenuated the inhibitory effect of CCK-8 (0.5 μmol·L-1) on CSB activity. Pretreatment with L-NAME (100 μmol·L-1), an inhibitor of NO synthase, did not affect the inhibitory action of CCK-8. CONCLUSION CCK-8 inhibits CSB activity, which may be mediated by activating CCK receptors in the carotid sinus area and thereby resulting in an inhibition of stretch-sensitive channels and decrease in Ca2+ influx.

The Role of the Vestibular System in Modulating Blood Pressure of Sinoaortic Denervated Rats

BACKGROUND AND OBJECTIVES: The vestibuloautonomic reflex controls respiration and blood pressure during locomotion. The purpose of this study was to investigate the role of the peripheral vestibular receptor in the control of blood pressure in sinoaortic denervated (SAD) rats. MATERIALS AND METHODS: The baroreceptor reflex was removed by SAD in labyrinthectomized rats. The expression of c-Fos protein in the vestibular nuclear complex, and other nuclei related to control of blood pressure, was measured following the induction of acute hypotension using sodium nitroprusside (SNP). RESULTS: The SNP induced acute hypotension, in intact labyrinthine rats, increased the expression of c-Fos protein in the supraoptic nucleus, paraventricular nucleus, rostral ventrolateral medulla, solitary nucleus, and vestibular nuclear complex. The expression of c-Fos protein, following the SNP induced acute hypotension in the SAD rats, increased the expression of c-Fos protein in the paraventricular nucleus, rostral ventrolateral medulla, and medial and inferior vestibular nuclei. The acute hypotension induced by SNP in a unilateral labyrinthectomy, with SAD, increased the expression of c-Fos protein in the contralesional vestibular nuclear complex, but decreased its expression in the ipsilesional vestibular nuclear complex. The acute hypotension induced by SNP in a bilateral labyrinthectomy, with SAD, showed only slight expression of c-Fos protein in the bilateral vestibular nuclear complex. CONCLUSION: These results suggest that the acute hypotension induced by SNP activates the vestibular nuclear neurons by decreasing the blood flow in the peripheral vestibular receptors, and that these in turn modulate blood pressure through activation of the catecholaminergic nervous system and neuroendocrine reflex.