Effects of intravenous AVP on cardiac output, mesenteric hemodynamics, and splanchnic nerve activity

To elucidate the effects of intravenous arginine vasopressin (AVP) on the neural control of the circulation, we investigated the action of AVP on neural circulatory control with respect to its influence on cardiac output (CO), mesenteric blood flow (MBF), and splanchnic nerve activity (SpNA) in conscious rats. We implanted Doppler flow probes and bipolar electrodes into seven Wistar rats for continuous monitoring of CO, MBF, and SpNa. After the infusion of four different equipressor doses of AVP and methoxamine, the decreases in heart rate (HR) and CO were significantly greater with AVP than with methoxamine. Pretreatment with atenolol and methscopolamine bromide abolished the decreases in HR after both AVP and methoxamine injections but attenuated the AVP-induced decreases in CO less than the methoxamine-induced CO decreases. In untreated rats and in rats receiving cardiac autonomic blockade, the reduction in MBF and the increases in mesenteric resistance were greater after AVP than after methoxamine. Furthermore, SpNA decreased to a greater extent with all doses of AVP than with methoxamine. We conclude that in the rat the exaggerated reduction in CO induced by circulating AVP is not because of a sensitization of neural mechanisms but rather to caridac actions of the peptide. In contrast, AVP sensitizes the sympathetic control of the mesenteric vascular bed to counterbalance its potent local vasoconstrictor effects.