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RESEARCH PRODUCT

Effects of vasopressin on human renal arteries

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description

The effects of vasopressin were studied in isolated rings from branches (2-3 mm in external diameter) of human renal arteries obtained from 18 patients undergoing nephrectomy for non-obstructive neoplasia. In arterial rings under resting tension, vasopressin produced concentration-dependent and endothelium-independent contractions with an EC 50 of 9.1 x 10 -10 mol L -1 . The vasopressin V 1 receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP (10 -6 mol L -1 ) displaced the control curve to vasopressin 564-fold to the right in a parallel manner. In precontracted arterial rings and previously treated with the V 1 antagonist (10 -6 mol L -1 ) vasopressin caused endothelium-independent relaxation. The relaxation to vasopressin was reduced significantly by indomethacin (10 -6 mol L -1 ) and unaffected by the V 1 /V 2 receptor antagonist desGly d(CH 2 ) 5 -D-Tyr(Et)ValAVP (10 -6 mol L -1 ) or by N G -nitro-L-arginine methyl ester (10 -4 mol L -1 ). These observations indicate that vasopressin is primarily a constrictor of human renal arteries by V 1 -receptor stimulation. Vasopressin causes prostaglandin-mediated dilatation of human renal arteries only if V 1 -receptor blockade is present. The effects of vasopressin on human renal arteries may be relevant in those clinical situations characterized by increased plasma vasopressin levels.