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RENAL DENERVATION ATTENUATES LONG‐TERM HYPERTENSIVE EFFECTS OF ANGIOTENSIN II IN THE RAT
Author(s) -
Hendel Michael D,
Collister John P
Publication year - 2006
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2006.04514.x
Subject(s) - medicine , denervation , blood pressure , baroreceptor , angiotensin ii , circumventricular organs , endocrinology , mean arterial pressure , reflex , kidney , anesthesia , sympathetic nervous system , renin–angiotensin system , central nervous system , heart rate
SUMMARY1 It is well accepted that some of the long‐term effects of angiotensin (Ang) II are mediated via the central nervous system. Some of these actions that are mediated by the circumventricular organs and the baroreceptor reflex are thought to then alter sympathetic nervous system activity. In particular, there is some debate as to the role of renal nerves in the chronic effects of AngII. The aim of the present study was to assess the contribution of the renal nerves in a long‐term model of progressive AngII‐induced hypertension. 2 Male Sprague‐Dawley rats were subjected to either bilateral renal denervation (RDX; n = 7) or sham surgery (SHAM; n = 8). Rats were instrumented with radiotelemetric transducers and venous catheters for the measurement of blood pressure and AngII infusion, respectively. A 4.0% NaCl diet and distilled water were provided ad libitum . The first 3 days served as the control period (7 mL/day, 0.9% NaCl, i.v.). This was followed by an infusion of AngII for 16 days (10 ng/kg per min, i.v.) and a 3 day recovery period identical to control. 3 Baseline arterial pressure between RDX and SHAM rats did not differ. Following AngII treatment, the arterial pressure of SHAM rats increased more rapidly than that of RDX rats. By Day 10 of treatment, the mean arterial pressure was significantly different between groups, having increased to 166 ± 4 mmHg in SHAM rats and 135 ± 11 mmHg in RDX rats. This trend continued for the remainder of AngII treatment. 4 The present results indicate that the renal nerves are necessary for the full expression of AngII‐induced hypertension.