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1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: sved{at}bns.pitt.edu.
The present study sought to determine whether an acute increase in arterial blood pressure (ABP) reduces plasma vasopressin (VP) levels stimulated by ANG II or hyperosmolality. During an intravenous infusion of ANG II (100 ng kg-1 min-1), attenuation of the ANG II-evoked increase in ABP with diazoxide or minoxidil did not further enhance plasma VP levels in rats. When VP secretion was stimulated by an infusion of hypertonic saline, co-infusion of the 
-adrenergic agonist phenylephrine (PE) significantly increased ABP but did not reduce plasma VP levels. In fact, plasma VP levels were enhanced. The enhancement of plasma VP levels cannot be explained by a direct stimulatory action of PE, as plasma VP levels of iso-osmotic rats did not change during a similar infusion of PE. An infusion of endothelin-1 in hyperosmotic rats significantly raised ABP but did not reduce plasma VP levels; rather, VP levels increased as observed with PE. In -chloralose anesthetized rats infused with hypertonic saline, inflation of an aortic cuff to increase ABP and stimulate arterial baroreceptors did not reduce plasma VP levels. In each experiment, plasma oxytocin levels paralleled plasma VP levels. Collectively, the present findings suggest that an acute increase in ABP does not inhibit VP secretion.
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