A STUDY OF ANGIOTENSIN-II RECEPTORS AFTER CHRONIC INHIBITION OF NITRIC-OXIDE SYNTHASE IN THE SPONTANEOUSLY HYPERTENSIVE RAT

1. Nitric oxide (NO) synthase inhibition, induces a sustained increase in blood pressure and amplifies the presser response to infused angio tensin II (AngII). This study was designed to investigate the contribu tion of AngII receptors to the elevated blood pressure and enhanced pr esser response to AngII in the spontaneously hypertensive rat (SHR) ch ronically 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 drinkin g water. Group II rats received water only. Blood pressure was monitor ed daily by tail-cuff plethysmography, Plasma AngII was measured by ra dioimmunoassay. Aortic and uterine receptor binding was determined by saturation analysis using [I-125]-Sar(8), Ile(1)) AngII, Data was anal ysed using the computer program LIGAND. 3. Mean systolic blood pressur e was significantly elevated in rats treated with L-NAME compared with the control group. Plasma AngII concentration was slightly decreased in rats treated with L-NAME compared with control, Densities of both a ortic 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 af finity was unchanged. 4. We conclude that the increased blood pressure and enhanced presser responsiveness that occurs with chronic inhibiti on of NO synthesis may result partly from increased vascular AngII rec eptor expression.