Vasopressin: mechanism of central cardiovascular action in conscious rats

Arginine vasopressin (AVP) and AVP binding sites have been localized in brain areas involved in cardiovascular control. To elucidate the mechanisms by which brain AVP may participate in central blood pressure regulation, we investigated the effects of central AVP receptor stimulation on mean arterial pressure (MAP), heart rate (HR), efferent splanchnic nerve (SpNA), and renal nerve activity (RNA) in conscious chronically instrumented rats. Intracerebroventricular (i.c.v.) injections of AVP (1-100 ng) produced dose-dependent increases in MAP together with marked increases in HR, SpNA, and RNA. The pressor responses were inhibited by peripheral alpha-adrenoceptor blockade with i.v. phentolamine. In contrast, the pressor responses to either i.v. or intracarotid injections of AVP were accompanied by baroreceptor reflex (BRR)-mediated decreases in HR and SpNA. Central (i.c.v.) pretreatment with d(CH2)5AVP, a V1-AVP receptor antagonist, completely abolished the responses to i.c.v. but not to i.v. AVP. The same antagonist had no effect on the responses to i.c.v. angiotensin II. Our results demonstrate that: (a) central AVP overrides the BRR by sympathetic stimulation, whereas blood-borne AVP activates the BRR; (b) specific AVP receptors in the brain probably of the V1-subtype are involved in the central pressor responses to AVP; (c) the central pressor actions of AVP are transmitted to the periphery by stimulation of the sympathetic nervous system. We conclude that brain AVP may contribute to central cardiovascular control by modulating the sympathetic outflow to the periphery.