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PROLONGED SYSTEMIC AND REGIONAL HAEMODYNAMIC EFFECTS OF INTRACEREBROVENTRICULAR ANGIOTENSIN II IN CONSCIOUS SHEEP
Author(s) -
May Clive N.
Publication year - 1996
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.1440-1681.1996.tb01137.x
Subject(s) - vasoconstriction , vasopressin , angiotensin ii , medicine , hemodynamics , blood pressure , endocrinology , plasma renin activity , renin–angiotensin system
SUMMARY 1. The haemodynamic mechanisms by which infusion of angiotensin II (AngII), either into the lateral cerebral ventricles (i.c.v.) or intravenously (i.v.), increased arterial pressure were studied in conscious sheep. 2. Sheep were previously fitted with flow probes for measurement of cardiac output and coronary, mesenteric, renal and iliac blood flows. 3. Intracerebroventricular AngII (10 nmol/h for 1 h) increased arterial pressure by 11 ± 4 mmHg (P < 0.001) due to vasoconstriction, predominantly in the mesenteric vasculature. These effects developed over 30 min and took 2 h to return to control. Following the infusion renal conductance increased continuously for 3 h, resulting in a parallel increase in renal blood flow (to 75 ± 18 mL/min above control, P<0.001). 4. Intracerebroventricular AngII increased plasma vasopressin from 0.8 ± 0.3 to 7.2 ± 1.8 pg/mL (P < 0.01), and reduced plasma renin concentration from 0.9 ± 0.3 to <0.4 nmol/L/h. 5. The pressor effect of i.v. AngII (5, 10, 25, 50 nmol/h) also depended on peripheral vasoconstriction, but the pattern of responses was different. The greatest degree of vasoconstriction occurred in the renal, followed by the mesenteric and iliac vascular beds; these effects were rapid in onset and offset. 6. In conclusion, the pressor responses to both i.c.v. and i.v. angiotensin depended on peripheral vasoconstriction, but there were contrasting regional haemodynamic changes. ICV AngII caused a prolonged pressor response, mainly due to mesenteric vasoconstriction possibly partly due to vasopressin release, and following the infusion there was a pronounced, long‐lasting renal vasodilatation. In contrast, i.v. AngII caused vasoconstriction preferentially in the renal vascular bed and its effects were short lasting.