EFFECTS OF VASOPRESSIN ON HUMAN RENAL-ARTERIES

The effects of vasopressin were studied in isolated rings from branche s (2-3 mm in external diameter) of human renal arteries obtained from 18 patients undergoing nephrectomy for non-obstructive neoplasia. In a rterial rings under resting tension, vasopressin produced concentratio n-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 vaso pressin 564-fold to the right in a parallel manner. In precontracted a rterial rings and previously treated with the V-1 antagonist (10(-6) m ol L(-1)) vasopressin caused endothelium-independent relaxation. The r elaxation to vasopressin was reduced significantly by indomethacin (10 (-6) mol L(-1)) and unaffected by the V-1/V-2 receptor antagonist desG ly d(CH2)(5)-D-Tyr(Et)ValAVP (10(-6) mol L(-1)) or by N-G-nitro-L-argi nine 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 dilat ation of human renal arteries only if V-1-receptor blockade is present . The effects of vasopressin on human renal arteries may be relevant i n those clinical situations characterized by increased plasma vasopres sin levels.