Cardiac weight in hypertension induced by nitric oxide synthase blockade.

Arnal, Jean‐François; Amrani, Abdelaziz; Châtellier, Gilles; Ménard, Joël; Michel, Jean‐Baptiste

doi:10.1161/01.hyp.22.3.380

Cited by 171 publications

(94 citation statements)

References 37 publications

(25 reference statements)

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“…In contrast, the Dahl saltsensitive rat, in which this hemodynamic adaptation is defective, develops severe glomerular injury. 44 As in previous studies of moderate hypertension, [45][46][47] gross hypertrophy of the left ventricle was not observed in rats that received neonatal PDTC. This finding also mimics observations made in human hypertensive subjects, a substantial proportion of which may show no clinical signs of left ventricular hypertrophy.…”

Section: Discussionsupporting

confidence: 64%

Programmed hypertension in rats treated with a NF-κB inhibitor during nephrogenesis: renal mechanisms

et al. 2011

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Suppression of the renin-angiotensin system (RAS) during murine lactation causes progressive renal injury, indicating a physiological action of angiotensin II on nephrogenesis. The nuclear factor NF-jB system is one of the main intracellular mediators of angiotensin II. We investigated whether inhibition of this system with pyrrolidine dithiocarbamate (PDTC) during rat nephrogenesis would lead to similar hypertension and renal injury as observed with RAS suppressors. Immediately after delivery, 32 Munich-Wistar dams, each nursing 6 male pups, were divided into 2 groups: C, untreated, and PDTC, receiving PDTC, 280 mg kg -1 day -1 orally, during 21 days. After weaning, the offspring were followed until 10 months of age without treatment. Adult rats that received neonatal PDTC exhibited stable hypertension and myocardial injury, without albuminuria. To gain additional insight into this process, the renal expression of RAS components and sodium transporters were determined by quantitative real-time PCR (qRT-PCR) at 3 and 10 months of life. Renal renin and angiotensinogen were upregulated at 3 and downregulated at 10 months of age, suggesting a role for early local RAS activation. Likewise, there was early upregulation of the proximal sodium/glucose and sodium/bicarbonate transporters, which abated later in life, suggesting that additional factors sustained hypertension in the long run. The conclusions drawn from the findings were as follows: (1) an intact NF-jB system during nephrogenesis may be essential to normal renal and cardiovascular function in adult life; (2) neonatal PDTC represents a new model of hypertension, lacking overt structural injury or functional impairment of the kidneys; and (3) hypertension in this model seems associated with early temporary activation of renal RAS and sodium transporters.

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Section: Discussionsupporting

confidence: 64%

Programmed hypertension in rats treated with a NF-κB inhibitor during nephrogenesis: renal mechanisms

et al. 2011

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“…However, reports of modification of tissue ACE activity during long-term ¬_NAME treatment are inconsistent in the literature: cardiac ACE activity was either increased or unchanged (Arnal et al 1993;Takemoto et al 1997). The molecular mechanism of the pro-growth property of Ang II involves both p42Ïp44 MAP kinase and p70 S6K activation (Sadoshima et al 1995) in addition to induction of c-fos and c-jun genes (Kudoh et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Effect of Captopril in L‐Name‐Induced Hypertension on the Rat Myocardium, Aorta, Brain and Kidney

Bernátová

Pecháňová

Šimko

1999

Experimental Physiology

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summary Long-term administration of N G -nitro-¬_arginine methyl ester (¬_NAME) induces development of hypertension and hypertrophy of the left ventricle in rats. The aim of the present study was to demonstrate the effect of chronic ¬_NAME treatment on DNA and RNA concentration, and protein synthesis in the rat heart, aorta, brain and kidney and to determine the effect of angiotensin converting enzyme (ACE) inhibitor captopril on these potential alterations. Four groups of rats were investigated: control, ¬_NAME (40 mg kg¢ day¢), captopril (100 mg kg¢ day¢), and ¬_NAME (40 mg kg¢ day¢) + captopril (100 mg kg¢ day¢). NO synthase activity in the heart, aorta, brain and kidney was found to be decreased in the ¬_NAME group. In the group of rats treated with ¬_NAME + captopril, captopril did not affect NO synthase inhibition. Captopril, however, completely prevented development of hypertension and left ventricular hypertrophy in this group. In the ¬_NAME group, DNA and RNA concentrations, as well as [14 C]leucine incorporation, were significantly increased in all the tissues investigated. In the ¬_NAME + captopril group, captopril completely prevented the enhancement of DNA and RNA concentrations and [ 14 C]leucine incorporation in all tissues compared to the ¬_NAME group. Moreover, a significant decrease in RNA concentration and [ 14 C]leucine incorporation below control values was found in the captopril group as well as the ¬_NAME + captopril group in all the tissues investigated. We conclude that captopril prevented the development of hypertension and increase in nucleic acid concentration and protein synthesis in the heart, aorta, brain and kidney in rats treated with ¬_NAME + captopril. However, this protective effect of captopril was not associated with increased NO synthase activity in this model of hypertension.

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“…However, the results regarding cardiac hypertrophy from L-NAME-treated animals are controversial. [6][7][8]27,28) These contradictory results may be related to the doses of L-NAME used and the duration of treatment. One study, which used a low dose of L-NAME (7.5 mg/kg/day) for 2, 4, and 6 months, reported a significant reduction in the left ventricular index in L-NAME-treated rats in spite of hypertension.…”

Section: )mentioning

confidence: 99%

Role of Nitric Oxide in the Progression of Cardiovascular Remodeling Induced by Carotid Arterio-Venous Shunt in Rabbits.

et al. 2003

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SUMMARYDespite a variety of biological roles for nitric oxide (NO) in the cardiovascular system, little is known about whether NO is involved in cardiac hypertrophy. We hypothesized that NO production following a sustained increase in shear stress by volumeoverload modifies the level of cardiac hypertrophy independent of hemodynamic changes. Volume-overload was induced by shunt formation between the left common carotid artery and the external jugular vein in 21 rabbits. These shunt rabbits were randomly assigned to 3 groups: shunt with no treatment (n=8), shunt treated with a low dose of N G -nitro-Larginine methyl ester (L-NAME, 0.5 g/L in drinking water, n=8), and shunt with a high dose of L-NAME (1.5 g/L, n=5). Eight sham operated rabbits were used as controls. Treatments were started immediately after operation and were continued for 6 weeks. Chronic volume-overload by shunt formation caused left ventricular dilatation and arterial enlargement proximal to the fistula. The relative wall thickness of the left ventricle was decreased, indicating eccentric cardiac hypertrophy. L-NAME elevated mean arterial blood pressure (P<0.01) and reduced the increment of cardiac output (P<0.05). L-NAME attenuated ventricular weight (P<0.01), ventricular cavity dilatation (P<0.01), and arterial enlargement (P<0.05). The re-capitulation of atrial natriuretic factor mRNA in the hypertrophied left ventricular myocardium by volume-overload was attenuated with L-NAME. In this model with chronic volume-overload, NO plays a pivotal role in the progression of cardiovascular remodeling by regulating the loading conditions of the heart. (Jpn Heart J 2003; 44: 127-137)

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Cardiac weight in hypertension induced by nitric oxide synthase blockade.

Cited by 171 publications

References 37 publications

Programmed hypertension in rats treated with a NF-κB inhibitor during nephrogenesis: renal mechanisms

Programmed hypertension in rats treated with a NF-κB inhibitor during nephrogenesis: renal mechanisms

Effect of Captopril in L‐Name‐Induced Hypertension on the Rat Myocardium, Aorta, Brain and Kidney

Role of Nitric Oxide in the Progression of Cardiovascular Remodeling Induced by Carotid Arterio-Venous Shunt in Rabbits.

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