Oral administration of L-arginine decreases blood pressure and increases renal excretion of sodium and water in renovascular hypertensive rats

Gouvêa, Sônia Alves; Moysés, Margareth Ribeiro; Bissoli, Nazaré Souza; Pires, J.G.P.; Cabral, Antônio M.; Abreu, Gláucia Rodrigues de

doi:10.1590/s0100-879x2003000700017

Cited by 20 publications

(21 citation statements)

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“…NOS substrate supplementation has beneficial effects on both blood pressure and renal disease in clinical trials (35,47,52) and in experimental models (12,14,27,32,40,42,50). In animals with ureteral obstruction, the administration of L-arginine increases GFR and renal blood flow to the postobstructed kidney and decreases the infiltration of macrophages of the renal parenchyma (29).…”

Section: Discussionmentioning

confidence: 99%

“…Reduced levels of L-arginine have been observed in renal failure, but the clinical relevance is uncertain, as the measured serum concentrations are well in excess of the K m for eNOS (1,38). Nevertheless, both clinical (20,47,52,60) and experimental studies (12,14,18,22,23,36,44) have demonstrated that substrate supplementation stimulates NO production and attenuates renal damage and salt-sensitive hypertension. Furthermore, chronic NO inhibition with N G -nitro-Larginine methyl ester (L-NAME), an antagonist for L-arginine, causes salt-sensitive hypertension and the development of renal injury (62).…”

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confidence: 99%

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Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals

Carlström¹,

Brown²,

Edlund³

et al. 2008

American Journal of Physiology-Renal Physiology

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Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals. Am J Physiol Renal Physiol 294: F362-F370, 2008. First published November 21, 2007 doi:10.1152/ajprenal.00410.2007.-Hydronephrotic animals develop renal injury and hypertension, which is associated with an abnormal tubuloglomerular feedback (TGF). The TGF sensitivity is coupled to nitric oxide (NO) in the macula densa. The involvement of reduced NO availability in the development of hypertension in hydronephrosis was investigated. Hydronephrosis was induced by ureteral obstruction in young rats. Blood pressure and renal excretion were measured in adulthood, under different sodium conditions, and before and after chronic administration of either N G -nitro-L-arginine methyl ester (L-NAME) or L-arginine. Blood samples for ADMA, SDMA, and L-arginine analysis were taken and the renal tissue was used for histology and determination of NO synthase (NOS) proteins. TGF characteristics were determined by stop-flow pressure technique before and after administration of 7-nitroindazole (7-NI) or L-arginine. Hydronephrotic animals developed salt-sensitive hypertension, which was associated with pressure natriuresis and diuresis. The blood pressure response to L-NAME was attenuated and L-arginine supplementation decreased blood pressure in hydronephrotic animals, but not in the controls. Under control conditions, reactivity and sensitivity of the TGF response were greater in the hydronephrotic group. 7-NI administration increased TGF reactivity and sensitivity in control animals, whereas, in hydronephrotic animals, neuronal NOS (nNOS) inhibition had no effect. L-Arginine attenuated TGF response more in hydronephrotic kidneys than in controls. The hydronephrotic animals displayed various degrees of histopathological changes. ADMA and SDMA levels were higher and the renal expressions of nNOS and endothelial NOS proteins were lower in animals with hydronephrosis. Reduced NO availability in the diseased kidney in hydronephrosis, and subsequent resetting of the TGF mechanism, plays an important role in the development of hypertension.ADMA; tubuloglomerular feedback; L-arginine; L-NAME; telemetry; blood pressure HYPERTENSION IS THE MOST COMMON chronic disorders worldwide and secondary forms of hypertension are found in 5-10% of the hypertensive population, of which most can be linked to renal disease (24). In humans, as well as in experimental models of salt-sensitive hypertension, there is a growing body of evidence pointing at a close relationship between nitric oxide (NO) deficiency and development of hypertension (37).Hydronephrosis due to obstruction at the level of the pelvicureteric junction is a common condition in children, with an incidence in newborns of ϳ1%. The obstruction is mostly partial and congenital of origin. Unilateral hydronephrosis causes salt-sensitive hypertension in both rats (5) and mice (7).The renal function in hydronephrotic animals, measured as renal blood flow and glomerular filtration rate (GFR), is rather...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals

Carlström¹,

Brown²,

Edlund³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…These results agree with the previous reports from Dumont et al [11] who found that a low dose instead a high dose of L-arginine in drinking water significantly attenuates the development of hypertension in uraemic rats. Gouvêa et al [10] supported the hypothesis that in WK rats with renovascular hypertension L-arginine treatment (300 mg/day during 14 days) decreases the arterial pressure (23%) in the two-kidney, one-clip (2K1C) renovascular hypertension model induced hypertension rats, not only because of the already known vasodilator effects of NO formation, but also because there is an increase in renal excretion of water and sodium; Kawano et al [24] reported a significant reduction (11.3%) in systolic pressure in fed rats supplemented with 1.4% Larginine [24]. Nevertheless, Chang et al [12] reported that early in vitro studies using aorta or artery segments isolated from genetic and secondary hypertensive animals suggested that endothelium-dependent relaxation of blood vessels was impaired in hypertension.…”

Section: L-arginine Hypolipidemic Activitymentioning

confidence: 99%

“…Many research have shown that intravenous or oral L-arginine administration increases NO synthesis and prevents endothelial dysfunction in animal models of pulmonary hypertension or salt-induced hypertension [5]. Gouvêa et al [10] used renovascular hypertensive rats, and reported that orally administered L-arginine acts in the rats kidney possibly inducing changes in renal hemodynamics or tubular transport due to an increase in NO formation. Dummont et al [11] found that a low dose (200 mg kg −1 ) instead a high dose (2,300 mg kg −1 ) of L-arginine in drinking water during 6 weeks, significantly attenuates the development of hypertension in uraemic rats.…”

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Effect of L-arginine Oral Supplementation on Response to Myocardial Infarction in Hypercholesterolemic and Hypertensive Rats

Piñeiro

Ortiz-Moreno

Mora‐Escobedo

et al. 2010

Plant Foods Hum Nutr

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The well known metabolic functions of L-arginine have been recently increased with the discovery of its role as the substrate for the synthesis of nitric oxide (NO), which has emerged as an endogenous signaling molecule with potential therapeutic implications for cardiovascular disease. Steady-state levels of NO are derived in part from dietary sources. It has been reported that supplementation of L-arginine reduces atherosclerosis in rabbits and reduces the arterial pressure in hypertensive rats. Therefore, we investigated the effect of L-arginine supplementation using a group of induced hypercholesterolemic rats and a group of spontaneously hypertensive rats; the infarcted area in cardiac tissue of both groups was measured during the response to myocardial infarction in the ischemia-reperfusion model. Hypercholesterolemic rats supplemented with 170 mg kg(-1) of L-arginine showed a significant (P

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“…Todos os animais foram sacrificados por eutanásia e submetidos à laparotomia exploratória para excisão do coração e pesagem dos ventrículos direito (VD) e esquerdo (VE, incluindo o septo), fígado, rim esquerdo (RE) e direito (RD) ): razão da massa do órgão pelo peso corpóreo (16,22) .…”

Section: íNdice De Hipertrofia Cardíaca Renal E Hepáticaunclassified

Uso crônico de decanoato de nandrolona como fator de risco para hipertensão arterial pulmonar em ratos Wistar

Graceli

Gava

Gomes

et al. 2010

Rev Bras Med Esporte

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RESUMOIntrodução: O uso indiscriminado de esteróides anabolizantes sintéticos, análogos à testosterona, implica aumento do risco cardiovascular e hipertrofia cardíaca. Assim, o aumento da massa ventricular direita corrigido pelo peso corporal (i.é., hipertrofia ventricular direita -HVD), poderia elevar o risco para o desenvolvimento de hipertensão arterial pulmonar (HAP). Objetivos: Examinar os efeitos do tratamento em longo prazo com decanoato de nadrolona na HVD e sua relação com a HAP em ratos. Métodos: 16 ratos Wistar com três meses de idade foram aleatoriamente divididos em dois grupos: 1) controle-sham (CONT, n = 8); 2) tratados com decanoato de nandrolona (DECA, n = 8). O tratamento consistiu na aplicação intramuscular de Deca-durabolin ® 6.0mg.kg -1 de peso corporal durante quatro semanas. Após tratamento, os animais foram anestesiados com hidrato de cloral (4.0mL.kg -1 , i.p.), submetidos à cateterização da artéria femoral para registro da pressão arterial media (PAM) e frequência cardíaca (FC). O coração, os rins e o fígado foram retirados, pesados e avaliados os índices de hipertrofia, os quais foram calculados pela razão da massa do órgão pelo peso corporal (mg.g -1 ). Resultados: Os animais tratados com DECA apresentaram aumento (p < 0,01) do peso corporal (338 ± 6g) vs. CONT (315 ± 5g). Não houve alterações da PAM, embora houvesse (p < 0,01) bradicardia nos animais tratados com DECA (321 ± 13bpm) vs. CONT (368 ± 11bpm). Verificou-se significativa (p < 0,01) hipertrofia dos ventrículos e rins, mas não no fígado. A correlação entre a HVD e PAM no grupo DECA apresentou coeficiente de Pearson positivo e maior (r 2 = 0,4013) quando comparado com o controle (r 2 = 0,0003). Conclusões: Esses dados demonstram que o uso em longo prazo de decanoato de nandrolona induz importante bradicardia e HVD, o que sugere aumento do risco para HAP.Palavras-chave: esteróide anabolizante, pressão sanguínea, hipertrofia ventricular, hipertensão arterial pulmonar. ABSTRACTIntroduction: The unsystematic use of anabolic steroids, synthetic analogs of testosterone, implies enhanced cardiovascular risk and cardiac hypertrophy. Thus, increased right ventricular mass corrected by the body weight (e.g.right ventricular hypertrophy -RVH) could raise the risk for development of pulmonary arterial hypertension (PAH). Objectives: to examine the effects of long-term chronic treatment with nandrolone decanoate on the RVH and its relationship with PAH in rats. Methods: 16 three-month Wistar male rats were treated with nandrolone decanoate (6.0 mg/kg -1 body weight; DECA, n=8) or control vehicle (CONT, n=8). The drug and vehicle were administered by a single injection in the femoral muscle once a week for 4 weeks. After the treatment, rats were anesthetized with chloral hydrate (4.0mL/kg

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Oral administration of L-arginine decreases blood pressure and increases renal excretion of sodium and water in renovascular hypertensive rats

Cited by 20 publications

References 24 publications

Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals

Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals

Effect of L-arginine Oral Supplementation on Response to Myocardial Infarction in Hypercholesterolemic and Hypertensive Rats

Uso crônico de decanoato de nandrolona como fator de risco para hipertensão arterial pulmonar em ratos Wistar

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