Effects of continuous converting enzyme blockade on renovascular hypertension in the rat

Freeman, R. H.; Davis, James O.; Watkins, Barry E.; Stephens, Gregory A.; DeForrest, Jack M.

doi:10.1152/ajprenal.1979.236.1.f21

Cited by 29 publications

(18 citation statements)

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“…Other investigators have also shown that captopril delays the onset of 1K1C hypertension for less than 8 days. 12 This is in agreement with reports that the acute high renin phase of 1K1C hypertension in rats lasts for no more than a week. 1718 Captopril lowered blood pressure in normotensive rats after 4 weeks of treatment, a finding in agreement with other studies.…”

Section: Control (N=8) Con-cap (N=3) M 1k1c-cap (N=4) Cd 1k1c (N=5) Osupporting

confidence: 92%

Captopril reduces aortic and microvascular growth in hypertensive and normotensive rats.

1990

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This experiment was designed to investigate the effect of converting enzyme inhibition on functional and structural vascular alterations in one-kidney, one clip hypertensive rats and in normotensive rats. Starting 1 day before surgery, 100 mg/kg/day captopril was given chronically to half of the hypertensive and normotensive groups in their drinking water. With use of intravital microscopy in the cremaster muscle, arteriolar dimensions were measured 4 weeks later, both before and after topical application of 10~3 M adenosine. Mean blood pressure was 124 ±4 mm Hg in control rats and 103 ±5 mm Hg in captopril-treated control rats (p<0.05). Mean blood pressure was significantly elevated to 183±5 mm Hg in captopril-treated one-kidney, one clip hypertensive rats and 193 ±5 mm Hg in one-kidney, one clip hypertensive rats. With use of histological techniques, a marked reduction of medial-intimal area of the abdominal aorta was found in captopril-treated control rats (24%), and hypertrophy of the aortic wall in one-kidney, one clip hypertensive rats was decreased 26% by captopril. Structural diameter reductions occurred in large arterioles of the captopril-treated control and hypertensive groups and the nontreated hypertensive group. In spite of a significant increase in wall-to-lumen ratio of first-order arterioles in all captopril-treated rats, captopril decreased cross-sectional wall area of these vessels 37% in hypertensive and 20% in control rats, respectively. Measured by stereological techniques, small arteriolar density decreased 30% in captopril-treated hypertensive rats and 17% in captopril-treated control rats. Therefore, smaller arteriolar lumens, decreased aortic and arteriolar cross-sectional wall area, and arteriolar rarefaction after converting enzyme inhibition, in spite of rising or falling blood pressure, are evidence that vascular growth was inhibited in vivo. {Hypertension 1990;15:68-77) T he influence of angiotensin II (Ang II) on vascular structure has been widely studied. Ang II has been shown to stimulate DNA and protein synthesis in cardiovascular tissue 1 and induce hypertrophy without cellular proliferation in cultured rat aortic smooth muscle cells (SMCs) maintained in a defined serum-free medium.2 Ang II also increased growth rates and cell size in cultured human SMCs grown in the presence of serum. However, all of these were in vitro studies. In vivo, captopril not only lowered blood pressure, but was more effective than hydralazine and propranolol in preventing increases in aortic SMC content, medial SMC weight, and percentage of polyploid SMCs in spontaneously hypertensive rats (SHR).4 SMC volume was also reduced in captopril-treated SHR and Wistar-Kyoto (WKY) rats. 4 In mesenteric arteries, captopril induced a long-lasting decrease in wallto-lumen (W/L) ratio in SHR and simultaneously induced long-lasting decreases in myocardial and aortic wall hypertrophy that persisted up to 7 weeks after treatment withdrawal.5 Recently, converting enzyme inhibition in two-kidney, one clip hypertensiv...

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Section: Control (N=8) Con-cap (N=3) M 1k1c-cap (N=4) Cd 1k1c (N=5) Osupporting

confidence: 92%

Captopril reduces aortic and microvascular growth in hypertensive and normotensive rats.

1990

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“…This suggests, but does not prove, that AngII receptors are upregulated in this model of hypertension. The initial elevation of blood pressure in the one-kidney Goldblatt model is also AngII-mediated [73] . Due to the absence of the other normal kidney, no compensatory increase in sodium and water excretion can occur, and hence, fluid volume is retained [74] .…”

Section: Pharmacologically-induced Hypertensionmentioning

confidence: 97%

Historic perspectives and recent advances in major animal models of Hypertension1

Sun

Zhang

2005

Acta Pharmacologica Sinica

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Hypertension and related cardiovascular diseases are the leading causes of death in many countries. The etiology of human essential hypertension is largely unknown. It is highly likely that hypertension is a complex and multifactorial disease resulting from the interaction of multiple genetic and environmental factors. Animal models of hypertension have been proved to be useful to study the pathogenesis of, and to find a new therapy for, hypertension. The aim of this article is to briefly review the most widely used rodent models of experimental hypertension, including history and recent advances. These models are classified as genetically-induced, environmentally-induced, pharmacologically-induced, and renalinduced hypertension according to the way of induction; the typical representatives of each of these major types of experimental hypertension are spontaneous hypertension, cold-induced hypertension, DOCA-salt-induced hypertension, and renal-induced hypertension, respectively. The processes of induction of hypertension, possible pathogenesis, characteristics, advantages, and limitations of these animal models are reviewed. In addition, the clinical implications of the above experimental models of hypertension are addressed.

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“…In rats with a normal contralateral kidney, surgically induced ischemia of the ipsilateral kidney (placement of a silver clip on one renal artery, i.e., 2-kidney-1-clip Goldblatt hypertension) causes the development of hypertension via a mechanism primarily dependent on the renin-angiotensin system. In 2-kidney-1-clip Goldblatt rats, plasma renin activity increases rapidly (1), and converting enzyme inhibition prevents the onset of hypertension (2,3). Further, the maintenance of an elevated arterial blood pressure in 2-kidney-I-clip Goldblatt rats depends on the renin-angiotensin system for some time after induction of hypertension.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II-noradrenergic interactions in renovascular hypertensive rats.

Zimmerman¹,

Robertson²,

Jackson³

1987

J. Clin. Invest.

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This study tested the hypothesis that interactions of endogenous angiotensin H (All) with the noradrenergic neuroeffector junction are important in renin-dependent hypertension. In the in situ blood-perfused rat mesentery, in normal rats exogenous All potentiated mesenteric vascular responses to periarterial (sympathetic) nerve stimulation (PNS) more than vascular responses to exogenous norepinephrine (NE). In 2-kidney-i-clip (2K-1C) rats with renovascular hypertension mesenteric vascular responses to PNS and NE were greater than in sham-operated rats, and renovascular hypertension mimicked the effects of exogenous All with respect to enhancing responses to PNS more than responses to NE. In 2K-iC rats, but not in sham-operated rats, i-Sar-8-Ile-AII markedly suppressed vascular responses to PNS, without influencing responses to NE. Finally, l-Sar-8-Ile-All attenuated sympathetic nerve stimulation-induced neuronal spillover of NE in 2K-iC rats, but not in sham-operated rats. These data indicate that renovascular hypertension enhances noradrenergic neurotransmission, and that this enhancement is mediated in part by AII-induced facilitation of NE release.

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Effects of continuous converting enzyme blockade on renovascular hypertension in the rat

Cited by 29 publications

References 0 publications

Captopril reduces aortic and microvascular growth in hypertensive and normotensive rats.

Captopril reduces aortic and microvascular growth in hypertensive and normotensive rats.

Historic perspectives and recent advances in major animal models of Hypertension1

Angiotensin II-noradrenergic interactions in renovascular hypertensive rats.

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