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Department of Pharmacology, The University of Missouri-Kansas City, Kansas City, Missouri 64108
Experiments were performed to determine if
glucocorticoids potentiate central hypertensive actions of ANG
II. Male Sprague-Dawley rats were treated for 3 days to 3 wk
with corticosterone (Cort). Experiments were performed in conscious
rats that had previously been instrumented with arterial and venous
catheters and an intracerebroventricular guide cannula in a lateral
ventricle. Baseline arterial pressure (AP) was greater in Cort-treated
rats than in control rats (119 ± 2 vs. 107 ± 1 mmHg,
P < 0.01). Microinjection of ANG II
intracerebroventricularly produced a significantly larger increase in
AP in Cort-treated rats than in control rats. For example, at 30 ng ANG
II, AP increased by 23 ± 1 and 16 ± 2 mmHg in Cort-treated
and control rats, respectively (P < 0.01).
Microinjection of an angiotensin type 1 receptor antagonist significantly decreased AP (
6 ± 2 mmHg) and heart rate
(26 ± 7 beats/min) in Cort-treated but not control rats.
Increases in AP produced by intravenous administration of ANG II were
not different between control and Cort-treated rats. Intravenous
injections of ANG II antagonist had no significant effects on mean AP
or heart rate in control or Cort-treated rats. Therefore, a sustained increase in plasma Cort augments the central pressor effects of ANG II
without altering the pressor response to peripheral administration of
the hormone.
corticosterone; hypertension; sympathetic nervous system; central nervous system; intracerebroventricular
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