AJP - Regulatory, Integrative and Comparative Physiology, Vol 245, Issue 6 881-R887, Copyright © 1983 by American Physiological Society
Effects of blockade of brain angiotensin II receptors in conscious, sodium-deprived dogs
V. L. Brooks and I. A. Reid
The present studies were designed to evaluate the physiological
significance of the actions of angiotensin II (ANG II) on the brain. The
effects of blockade of brain ANG II receptors by intracarotid or
intravertebral infusions of saralasin were studied in conscious dogs with
high circulating ANG II levels (142 +/- 16 pg/ml) due to a low-sodium diet.
Three doses of saralasin were infused into each pair of arteries and
intravenously: 0.1, 0.3, and 1.0 micrograms X kg-1 X min-1. Saralasin
produced dose-related decreases in arterial pressure during infusion into
the carotid or vertebral arteries, confirming that ANG II maintains
arterial pressure during sodium deficiency. However, intravenous saralasin
administration decreased pressure to a similar degree, suggesting that the
hypotensive effect was due to recirculation of saralasin, rather than to
blockade of a central action of circulating ANG II. Heart rate was not
altered by infusion of saralasin by any route. Saralasin administration
also caused a dose-dependent increase in plasma renin activity and plasma
ANG II concentration. However, because the increases produced by
intracarotid or intravertebral saralasin did not differ from the increase
produced by intravenous infusion, these results do not provide evidence
that renin release is modulated by a central action of ANG II during sodium
deficiency. Plasma corticosteroid levels were reduced (2.4 +/- 0.5 to 1.4
+/- 0.2 micrograms/dl, P less than 0.05) by intravenous infusion of the
highest dose of saralasin, but neither intracarotid nor intravertebral
saralasin infusion altered plasma corticosteroid concentration.(ABSTRACT
TRUNCATED AT 250 WORDS)
