Modulation of cardiovascular reflexes by arginine vasopressin

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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. A higher dose (3.7 pmol∙kg−1∙min−1) raised plasma levels to 268 ± 38 fmol/mL, decreased pulse pressure, increased central venous pressure (from 2.6 ± 0.5 to 4.1 ± 0.4 mmHg) (1 mmHg = 133.3 Pa) and suprisingly, in view of its direct vasoconstrictor effect, increased forearm blood flow by 30% and decreased forearm vascular resistance from 24 ± 4 to 18 ± 3 units (p < 0.05); mean arterial pressure was unchanged. The reflex vasodilator response to the sudden release of lower body negative pressure was augmented by AVP, whereas reflex changes in heart rate were unaltered. To test the hypothesis that vasopressin caused this resting vasodilation through inhibition of sympathetic nerve activity, we recorded postganglionic efferent muscle sympathetic nerve activity directly from the peroneal nerve before, during, and after intravenous infusion of AVP, 3.7 pmol∙kg−1∙min−1. Forearm vascular resistance again fell; sympathetic nerve activity decreased abruptly on starting AVP, from 254 ± 40 to 163 ± 34 units (p < 0.05), and remained below control throughout the infusion. This decrease did not appear to be due to a ganglionic action of AVP. The inhibition of sympathetic nerve activity probably resulted principally from mechanical stimulation of cardiac and arterial baroreceptors. However, since the marked reduction of nerve activity was not consistently associated with increases in arterial pressure or central venous pressure, we cannot exclude the possibility that vasopressin decreased sympathetic nerve activity in part by sensitizing baroreceptor afferents or by a central neural action. Sympathoinhibition would appear to be an important mechanism by which the potent pressor effects of AVP are countered in normal humans.

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