Modulation of cardiovascular reflexes by arginine vasopressin

Abstract

Arginine vasopressin (AVP), a potent vasoconstrictor, does not raise arterial pressure in normal humans or neurally intact animals, even during infusions that achieve pathophysiological plasma concentrations. It has been proposed that this is because AVP facilitates the baroreflex control of the circulation. We performed a series of investigations to test this hypothesis, and to determine sites at which AVP might act to augment the baroreflex. In anesthetized rabbits, vasopressin (36 pmol.kg-1.min-1) increased discharge from both medullated and nonmedullated single fibres from aortic baroreceptor nerves during elevations in aortic arch pressure. Similarly, vasopressin (36 pmol.kg-1.min-1) increased the response of left ventricular mechanoreceptor single fibre discharge to elevations of left ventricular end-diastolic pressure. These observations suggest that sensitization of high and low pressure baroreceptors is one mechanism by which vasopressin may facilitate baroreflexes. In a further series of experiments in sinoaortic denervated anesthetized rabbits, vasopressin (18 pmol.kg-1.min-1) facilitated vagally mediated reflex inhibition of renal sympathetic nerve activity during volume expansion. In humans, AVP (0.37 pmol.kg-1.min-1) raised plasma AVP to an antidiuretic level (22 +/- 4 fmol/mL), but did not change blood pressure or the baroreflex control of heart rate or forearm vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)