Reduction of kidney damage by supplementation of vitamins C and E in rats with deoxycorticosterone-salt-induced hypertension

We assessed whether cosupplementation of vitamins C and E has additive beneficial effects on reducing the kidney damage and attenuation of the arterial pressure elevation compared to administration of either vitamin C or vitamin E alone in deoxycorticosterone acetate-salt-induced hypertension. Forty rats were divided into 4 study groups and 1 sham-operated group. Unilateral nephrectomy was carried out in the study groups and hypertension was induced by deoxycorticosterone injection and 1% sodium chloride and 0.2% potassium chloride added to the drinking water. Vitamins C and E [200 mg/kg/day] or combination of them were administered with DOCA-salt for 4 weeks in 3 study groups. The effects of DOCA and salt and treatment with vitamins were compared in terms of blood pressure, urinary protein excretion, antioxidant activity of the kidneys, and renal histological changes. Four weeks of supplementations of vitamins C, vitamin E, and both in the DOCA-salt-treated rats had comparable significant effects in decreasing systolic blood pressure. Urinary protein excretion and histological damage did not significantly change with the combination therapy of vitamins C and E compared to the vitamin C or E alone. The renal levels of glutathione and ferric reducing/antioxidant power in combination therapy group were similar to the two other treatment groups and were significantly higher than non-treated group. Co-administration of vitamin C and E does not have an additive beneficial effect on reducing the kidney damage and hypertension compared to either vitamin C or E alone in DOCA-salt-induced hypertension

Acute AT1 receptor blockade does not improve the depressed baroreflex in rats with chronic renal hypertension

To assess the role of angiotensin II in the sensitivity of the baroreflex control of heart rate (HR) in normotensive rats (N = 6) and chronically hypertensive rats (1K1C, 2 months, N = 7), reflex changes of HR were evaluated before and after (15 min) the administration of a selective angiotensin II receptor antagonist (losartan, 10 mg/kg, iv). Baseline values of mean arterial pressure (MAP) were higher in hypertensive rats (195 ± 6 mmHg) than in normotensive rats (110 ± 2 mmHg). Losartan administration promoted a decrease in MAP only in hypertensive rats (16 percent), with no changes in HR. During the control period, the sensitivity of the bradycardic and tachycardic responses to acute MAP changes were depressed in hypertensive rats (~70 percent and ~65 percent, respectively) and remained unchanged after losartan administration. Plasma renin activity was similar in the two groups. The present study demonstrates that acute blockade of AT1 receptors with losartan lowers the MAP in chronic renal hypertensive rats without reversal of baroreflex hyposensitivity, suggesting that the impairment of baroreflex control of HR is not dependent on an increased angiotensin II level

Erythropoietin does not affect nitric oxide system in rats with chronic renal failure

We investigated to see whether an altered role of nitric oxide (NO) system is involved in erythropoietin (EPO)-induced hypertension in chronic renal failure (CRF). Male Sprague-Dawley rats were five-sixths nephrectomized to induce CRF. Six weeks after the operation, EPO or vehicle was injected for another 6 weeks. Plasma and urine nitrite/nitrate (NOx) levels were determined. Expression of NO synthase (NOS) proteins in the aortae and kidneys were also determined. In addition, the isometric tension of isolated aorta in response to acetylcholine and nitroprusside was examined. Blood pressure progressively rose in CRF groups, the degree of which was augmented by EPO treatment. Plasma NOx levels did not differ among the groups, while urine NOx levels were lower in CRF groups. Endothelial NOS expression was lower in the kidney and aorta in CRF rats, which was not further affected by EPO-treatment. The inducible NOS expression in the kidney and aorta was not different among the groups. Acetylcholine and sodium nitroprusside caused dose-dependent relaxations of aortic rings, the degree of which was not altered by EPO-treatment. Taken together, EPO-treatment aggravates hypertension in CRF, but altered role of NO system may not be involved.

Hypertension and the kidneys--inter-relationship and therapeutic approach.

Over the last decade, a great body of evidence has pointed towards the role of kidneys in the genesis and maintenance of a hypertensive state. There exists a relationship between a rise in the blood pressure and a proportionate increase in the urinary excretion of sodium and water called the pressure-natriuresis curve. Chronic renal diseases are the most common causes of secondary hypertension accounting for 2-5% of all cases of secondary hypertension. The prevalence rate of renovascular hypertension based upon referral patterns range from 0.2% to 10% of hypertensive population. The data provided by the International Registries on end-stage renal disease have suggested that essential hypertension is an important cause of progressive renal damage. The pathological lesion observed in malignant hypertension is fibrinoid necrosis of the small arteries and arterioles. Amongst the armamentarium of antihypertensive drugs calcium channel antagonists and the angiotensin converting enzyme inhibitors have a role in limiting glomerular hypertension. The best modality to prevent and treat renal dysfunction in the presence of hypertension is an adequate and effective control of high blood pressure.

Efeito do urapidil sobre a pressão arterial, hemodinâmica renal, metabolismo lipídico e glicídico / The effect of urapidil on blood pressure, renal hemodynamics, lipid and glucose metabolism

PURPOSE--To evaluate the effects of urapidil on blood pressure (BP), renal hemodynamics and lipid and glucose metabolism, in patients with mild-to-moderate uncomplicated essential hypertension. METHODS--Fifteen hypertensive patients, aged 38-64 year-old were studied by ambulatory blood pressure monitoring system (ABPM). It was also evaluated: 1) the creatinine clearance; 2) the effective renal plasma flow by use of a single plasma sample after injection of orthoiodohippurate; 3) the serum triglycerides, cholesterol, and HDL-cholesterol; 4) blood levels of glucose and insulin. The urapidil dose ranged from 60 to 180 mg/day, according to the individual response. RESULTS--The values after four weeks washout-placebo and active treatment with urapidil showed: the systolic/diastolic BP was reduced from 157.7 +/- 6/108.0 +/- 2 on placebo to 140.4 +/- 4/97.3 +/- 3 mmHg (p < 0.05/p < 0.01) after urapidil, respectively, whereas heart rate was unchanged. The percentage of elevated systolic and diastolic BP values during 24h (BP load) was reduced from 60.9 to 54.4 and from 60.8 to 50.3, respectively. Effective renal plasma flow, glomerular filtration rate, filtration fraction and renal vascular resistance were unaltered by treatment. Significant increase in HDL-cholesterol was observed (from 39.5 +/- 3.6 on placebo vs 49.2 +/- 4.8 mg/dl (p < 0.01) after urapidil. Total cholesterol, LDL-cholesterol and triglycerides levels were not modified with treatment. Circulating plasma glucose and insulin remained unchanged. CONCLUSION--Urapidil is an effective antihypertensive agent without deleterious effect on renal hemodynamics, lipid and glucose metabolism.

Objetivo − Avaliar os efeitos do urapidil sobre a pressão arterial, hemodinâmica renal, metabolismo lipídico e glicídico em portadores de hipertensão arterial sistêmica primária leve a moderada. Métodos − Foram analisados 15 pacientes hipertensos, com idades entre 38 e 64 anos, utilizando-se a técnica da monitorização ambulatorial da pressão arterial (MAPA) em 24h, avaliando-se, também, os clearances de creatinina e do hipuran radioativo, espectrofotometria de cristal sólido e as dosagens do colesterol e triglicérides séricos, do HDL-colesterol, da glicemia e insulina. As doses de urapidil variaram de 60 a 180mg/dia, administradas 2 ou 3 vezes, de acordo com cada caso. A avaliação durou pelo menos 6 semanas. Resultados − Os parâmetros analisados após 4 semanas de washout-placebo e tratamento com urapidil revelaram: 1) redução significante das pressões sistólica e diastólica (157,7±6 e 108±2 na fase placebo para 140,4±4 e 97,3±3mmHg, p<0,05; p<0,01, respectivamente); 2) o fluxo plasmático renal efetivo, ritmo de filtração glomerular, fração de filtração e resistência vascular renal não sofreram mudanças significantes; 3) aumento significante na concentração sérica das HDLcolesterol (39,5±3,6 para 49,2±4,8mg/dl, p<0,01), sem modificações nos níveis séricos do colesterol total, LDL colesterol e triglicérides; 4) as curvas glicêmicas e insulínicas não se alteraram. Conclusão − O urapidil reduziu a pressão arterial sem promover alterações na hemodinâmica renal, metabolismo lipídico e glicídico

Role of kinins in the acute antihypertensive effect of enalapril in hypertensive rats

1. We used the kinin antagonist HOE 140 to investigate the role of endogenous kinins in the acute antihypertensive effect of the angiotensin converting enzyme inhibitor enalapril in chronic and acute renal hypertensive rats. 2. In normotensive rats, treatment with HOE 140 (33 micrograms/kg, sc) caused a complete blockade of the depressor effect of bradykinin (100 ng, ia) without affecting the depressor effect of sodium nitroprusside (1 microgram, i.v.) or the basal blood pressure. 3. HOE 140 treatment (33 micrograms/kg, sc, plus 330 ng/min, i.v.) did not affect basal blood pressure of chronic (6-7 weeks) one-kidney, one clip and two-kidney, one clip hypertensive rats and in rats with acute hypertension, elicited by unclamping the renal pedicle that had been occluded for 5 h, but HOE 140 completely blocked the hypotensive response to bradykinin (100 ng, ia) during the 60-min period after enalapril administration (2 mg/kg, i.v.). 4. Acutely hypertensive rats treated or not with HOE 140 (33 micrograms/kg, sc, plus 330 ng/min, i.v.) presented a similar fall in blood pressure after enalapril (165 +/- 5 to 137 +/- 6 mmHg and 166 +/- 5 to 136 +/- 6 mmHg, respectively). 5. Untreated two-kidney, one clip hypertensive rats presented a rapid and sustained fall in blood pressure after enalapril (177 +/- 4 to 148 +/- 4 mmHg) that did not differ from the HOE 140-treated (33 micrograms/kg, sc, plus 330 ng/min, i.v.) group (177 +/- 6 to 154 +/- 4 mmHg). 6. One-kidney, one clip hypertensive rats treated with HOE 140 (33 micrograms/kg, sc, plus 330 ng/min, i.v.) showed a significantly smaller fall in blood pressure after enalapril (204 +/- 7 to 179 +/- 9 mmHg) compared to the untreated rats (197 +/- 7 to 149 +/- 2 mmHg). 7. These results indicate that kinin potentiation plays an important role in the antihypertensive effect of acutely administered angiotensin converting enzyme inhibitor in the one-kidney, one clip model of hypertension.

Funçäo ventricular de animais submetidos a ablaçäo da massa renal: efeito do controle da pressäo arterial / Ventricular function in animals subjected to renal mass ablation: effect of blood pressure control

A determinaçäo da hipertrofia ventricular na insuficiência renal crônica é multifatorial. Foram estudadas a pressäo arterial da cauda, peso cardíaco, máxima pressäo desenvolvida e as relaçöes pressäo-volume de animais com ablaçäo de5/6 de massa renal, cuja pressäo arterial se mantinha elevada (IRC; n=16) ou que recebiam furosemida na dose de 16mg/Kg para controlar a pressäo (IRC-F; n=17). Animais submetidos a cirurgia fictícia serviram como controles (SHAM; n=15). Os animais que sofreram ablaçäo da massa renal apresentavan níveis de creatinina sérica maiores do que os näo-operados )IRC = 1,81 ñ 0,05; IRC - F = 1,75 ñ 0,08; SHAM = 0,72 ñ 0,09; p 0,001). A massa cardíaca estava aumentada nos grupos IRC hipertenso (0,99 ñ 0,02g) e normotenso (1,01 ñ 0,02g) comparativamente ao SHAM (0,84 ñ 0,01) [p < 0,01]. A máxima pressäo desenvolvida durante a oclusäo transitória da aorta foi semelhante nos três grupos (IRC = 221,2 ñ 7,04; IRC-F = 255,7 ñ 10,01; SHAM = 239,9 ñ 5,5 mmHg, n.s.). Entretanto, o volume diastólico final operacional dos grupos IRC-H e IRC-N (91,4 ñ 9,44; 70,9 ñ 6,22µl, respectivamente) eram significativamente maiores do que o observado no grupo SHAM (28,75 ñ 3,12µL, p < 0,001). Portanto, a HVE induzida pela uremia näo é dependente da hipertensäo arterial que acompanha esta condiçäo. Ainda, o rendimento sistólico dos animais com hipertrofia é semelhante ao dos animais normais, mas, aparentemente, depende de uma maior utilizaçäo do mecanismo de Frank-Starling para seu funcionamento normal

Nefrolitotomía anatrófica, tratamiento anestésico y protección renal: presentación de un caso / Anatrophic nephrolithotomy, anesthetic treatment and renal protection: a case report

Cuando se hace la oclusión vascular durante la nefrolitotomía antrófica, se precipitan modificaciones locales consecutivas al metabolismo anaeróbico; en estas condiciones se incrementa fundamentalmente el consumo de adenosintrifosfato cuya producción a su vez se minimiza. Al reinstalarse la circulación se movilizan sustancias vasoactivas deletéreas por el riñón. Es posible prevenir el daño renal mediante hipotermia local y perfusión de manitol y nifedipina, como se procuró en el caso clínico aquí comunicado

Diurético de alça no manuseio da hipertensäo arterial de glomerulonefrite difusa aguda pós-infecciosa / Lopp diuretic in haldling arterial hypertension of post infectious acute glomerulonephritis

Foram estudados 74 pacientes com síndrome nefrítico agudo. Estes pacientes eram portadores de glomerulonefrite difusa aguda pós infecciosa. Os pacientes foram estudados na primeira semana da sua doença. atendidos no Serviço de Pediatria do Hospital Universitário da Universidade Federal de Juiz de Fora. Cinqüenta e oito (58) pacientes com hipertensäo arterial significativa, diastólica acima do percentil 95, foram internados (Grupo I). Foram tratados com repouso, dieta hipossódica e furosemide. O furosemide foi usado na dose 2 a 7.5 mg-Kg-dose (3.94 + ou - 1.28 mg-Kg-dose); 16 pacientes foram acompanhados ambulatorialmente (Grupo II), levando em consideraçäo a pouca gravidade do seu quadro clínico; a pressäo arterial diastólica estava abaixo do percentil 95. Este grupo foi tratado com repouso e dieta hipossódica. Os dois grupos foram observados por 72 horas, em protocolos específicos. Concluiu-se que o furosemide baixou a pressäo arterial dos pacientes do Grupo I sem provocar diurese significativa quando comparados com pacientes do Grupo II. Os autores acreditam que o furosemide apresentou uma açäo vasodilatadora sistêmica, proporcional a degradaçäo da PGE2. Esta preservaçäo da PGE2 modularia a intensidade da vasodilataçäo