Angiotensin Sensitivity and Prostaglandins in Dogs with Renal Hypertension

Watson, Michael; McCormick, Janice; Ungar, A.

doi:10.1097/00004872-198410000-00006

Cited by 3 publications

(1 citation statement)

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“…In models unassociated with the administration of pressor agents, such as two kidney one-clip hypertension, there was no increase in pressor responsiveness to infused AngII. 15 Further, the administration of other pressor agents, such as ACTH, cyclosporin A and vasopressin, is associated with either no change in pressor sensitivity'6 or a decrease in pressor ~ensitivity.1~2'8 Thus, it is possible that this represents a direct effect of NO, whereby locally produced N O acts to decrease AngII receptor expression. Treatment with L-NAME, by decreasing NO production, may therefore prevent receptor down-regulation.…”

Section: Discussionmentioning

confidence: 99%

A Study of Angiotensin Ii Receptors After Chronic Inhibition of Nitric Oxide Synthase in the Spontaneously Hypertensive Rat

Yang

Macdonald

Duggan

1996

Clin Exp Pharma Physio

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1. Nitric oxide (NO) synthase inhibition, induces a sustained increase in blood pressure and amplifies the pressor response to infused angiotensin II (AngII). This study was designed to investigate the contribution of AngII receptors in the elevated blood pressure and enhanced pressor response to AngII in the spontaneously hypertensive rat (SHR) chronically treated with N(G)-nitro-L-arginine-methyl ester (L-NAME). 2. Two groups of 13 week old female SHR were housed four to a box. Group I rats received L-NAME for 7 days (2.5 mg/kg per day) in their drinking water. Group II rats received water only. Blood pressure was monitored daily by tail-cuff plethysmography. Plasma AngII was measured by radioimmunoassay. Aortic and uterine receptor binding was determined by saturation analysis using [125I]-Sar8, Ile1)AngII. Data was analysed using the computer program LIGAND. 3. Mean systolic blood pressure was significantly elevated in rats treated with L-NAME compared with the control group. Plasma AngII concentration was slightly decreased in rats treated L-NAME compared with control. Densities of both aortic and uterine AngII receptors increased significantly following NO synthase inhibition. Receptor affinity in the aorta decreased in the L-NAME group compared with control. However, uterine AngII receptor affinity was unchanged. 4. We conclude that the increased blood pressure and enhanced pressor responsiveness that occurs with chronic inhibition of NO synthesis may result partly from increased vascular AngII receptor expression.

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Section: Discussionmentioning

confidence: 99%