Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect.
OBJECTIVES: To assess which vasopressin receptor subtype mediates the vasodilation occurring in response to arginine vasopressin and 1-desamino-8-D (DD)-arginine vasopressin and whether nitric oxide is involved in these effects. MATERIALS AND METHODS: Vasoactive effects of arginine vasopressin and DD-arginine vasopressin on forearm vasculature were studied in healthy subjects and in patients with congenital nephrogenic diabetes insipidus with a vasopressin type 2 (V2) receptor gene defect. Venous occlusion plethysmography was used to assess the forearm blood flow responses to the infusion of arginine vasopressin and its analogue into the brachial artery, in the presence and the absence of the nitric oxide synthase inhibitor L-NG-monomethyl-arginine (L-NMMA). RESULTS: In healthy subjects (n =10), DD-arginine vasopressin (0.1, 1 and 10 or 5, 10 and 20 ng/min per dl) induced a dose-related increase in forearm blood flow, but did not affect forearm blood flow in the patients with nephrogenic diabetes insipidus (n = 3). In two healthy subjects, seven increasing doses of arginine vasopressin (0.25-12 ng/min per dl) induced an initial decrease in forearm blood flow and then a gradual increase. In one of the patients, the same arginine vasopressin doses produced a persistent decrease in forearm blood flow. In the healthy subjects, infusion of L-NMMA reduced forearm blood flow significantly (n = 10). Subsequent administration of DD-arginine vasopressin during L-NMMA infusion produced a slight reduction in the forearm blood flow increase compared with DD-arginine vasopressin alone, but this was significant only for the absolute forearm blood flow increase induced by 10 ng/min per dl in all subjects. Infusion of arginine vasopressin in the presence of L-NMMA did not increase forearm blood flow significantly. CONCLUSIONS: In human forearm vasculature, extrarenal V2 receptors mediate the vasodilation induced by DD-arginine vasopressin or high doses of arginine vasopressin, whereas these receptors are not necessary for arginine vasopressin-induced vasoconstriction. The DD-arginine vasopressin-induced vasodilation seems to be mediated predominantly by a mechanism other than endothelial nitric oxide release, whereas arginine vasopressin-induced vasodilation seems to involve nitric oxide release only.[1]References
- Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect. van Lieburg, A.F., Knoers, N.V., Monnens, L.A., Smits, P. J. Hypertens. (1995) [Pubmed]
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