Osmotically released vasopressin augments cardiopulmonary reflex inhibition of the circulation.

Exogenous arginine vasopressin (AVP) has been shown to augment the inhibitory influence of arterial and cardiopulmonary baroreflexes. This study examined the influence of osmotically released AVP on the inhibitory responses to activation of cardiopulmonary receptors by administration of veratrum alkaloids. Three groups of conscious dogs, with carotid sinus intact, with prior sinoaortic denervation (SAD), and with prior lesion of the area postrema (AP), were instrumented for monitoring arterial pressure and heart rate and with left circumflex coronary artery or left atrial catheters for administration of veratrum alkaloids. Conscious dogs were administered veratridine (0.5-1.0 microgram.kg-1.min-1) under control conditions, after infusion of hypertonic saline (HS, 6% NaCl), and after HS in the presence of the AVP vascular (V1) receptor antagonist. In carotid sinus-intact dogs, veratridine reduced arterial pressure (-10 +/- 0.4 mmHg). After HS infusion, the depressor response to veratridine was significantly greater (-18 +/- 0.8 mmHg). The enhanced depressor response during HS infusion was prevented by administration of the AVP antagonist (-8 +/- 0.6 mmHg). Responses to veratrum alkaloids in SAD dogs were similar. In AP-lesioned animals, the depressor effects of veratridine (-9 +/- 0.5 mmHg) were similar to intact animals. However, the response to veratridine during HS was not altered (-9 +/- 0.8 mmHg) in AP-lesioned dogs. Results suggest that osmotically stimulated AVP augments the inhibitory effects of cardiopulmonary reflexes and that this effect is mediated through the area postrema via the V1 receptor.