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1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260; 2 Department of Physiology and Medical Biophysics, Uppsala University, Uppsala 75123, Sweden; and 3 Department of Physiology, University of Odense, Odense DK-5000, Denmark
Arterial hypotension and hypovolemia
are known to stimulate neurohypophysial secretion of oxytocin (OT) in
rats, although the physiological function of OT under these
circumstances is uncertain. We now report that OT infused intravenously
into conscious rats at 125 ng · kg
1 · h
1,
a dose selected to mimic plasma OT levels during hypotension or
hypovolemia, increased plasma renin concentration and plasma renin
activity by twofold. This effect was prevented by systemic pretreatment
with an OT receptor antagonist {[1-(3-mercaptopropionic acid)-2-O-ethyl-D-Tyr-Thr4-Orn8]-OT}.
The OT antagonist did not block renin secretion induced by systemic
injection of the
-adrenergic receptor agonist isoproterenol, indicating that the OT antagonist does not interfere nonselectively with renin release. Pretreatment of rats with the
-adrenergic receptor antagonist nadolol also prevented OT-induced renin secretion. Similarly, nadolol injected during infusion of OT markedly reduced the
elevated plasma renin levels. These observations raise the possibility
that pituitary OT secretion during hypotension or hypovolemia in rats
may serve to support blood pressure by enhancing activation of the
renin-angiotensin system via a
-adrenergic receptor-dependent mechanism.
hypotension;
-adrenergic receptors; isoproterenol; nadolol
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