Hypertension, Vol 13, 463-468, Copyright © 1989 by American Heart Association
I Antonipillai, MI Broers and D Lang
Direct effects of dopamine on renin release were examined using static
incubations and perifusions of rat renal cortical slices. Dopamine (10(-
5)M) significantly stimulated renin release compared with control. To
determine which receptors are involved in dopamine-elicited renin release,
studies were performed with specific dopamine-1 and dopamine-2 receptor
agonists and antagonists, as well as with alpha- and beta- adrenergic
antagonists. Fenoldopam, a dopamine-1 receptor agonist, dose dependently
stimulated renin secretion both in static incubations and perifusions;
whereas quinpirole (10(-7)-10(-5)M), a dopamine-2 receptor agonist, was
ineffective. Phentolamine (10(-4)M), an alpha-adrenergic antagonist, did
not alter dopamine- or fenoldopam-induced renin release. Similarly,
propranolol, a beta-blocker, did not interfere with the renin stimulation
of dopamine (10(-5)M) or fenoldopam (10(-6)M) incubations or perifusion
experiments; whereas propranolol significantly blocked isoproterenol
action. SCH 23390 (10(-5)M), a specific dopamine-1 antagonist, blocked
dopamine- and fenoldopam- induced renin. In contrast, pimozide, a
dopamine-2 receptor antagonist, was ineffective. These studies indicate
that dopamine is a direct renin secretogogue, and its effects seem to be
mediated by specific dopamine- 1 receptor activation, as neither alpha- nor
beta-adrenergic blockers nor dopamine-2 receptor antagonists altered
dopamine actions. The results suggest that dopamine produced locally in the
kidney may stimulate renin secretion directly by dopamine-1 receptor
activation.
ARTICLES
Evidence that specific dopamine-1 receptor activation is involved in dopamine-induced renin release
Section of Endocrinology, LAC/USC Medical Center, 90033.
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