Responses to vasopressin and desmopressin of human cerebral arteries.

The effects of vasopressin and deamino-8-D-arginine vasopressin (desmopressin) were studied in isolated rings from branches (0.8-1.2 mm in external diameter) of human middle cerebral arteries obtained during autopsy of 27 patients who had died 3 to 10 hr before. In arterial rings under resting tension, vasopressin produced concentration-dependent contractions with an EC50 of 7.2 x 10(-10) M. The vasopressin V1 receptor antagonist [(1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2- (O-methyl)-tyrosine-8-arginine)vasopressin] (10(-6) M) displaced the control curve to vasopressin 1250-fold to the right in a parallel manner. The mixed V1-V2 receptor antagonist [(1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2- (O-ethyl)-D-tyrosine-4-valine-8-arginine-9-desglycine)vasopressin] (10(-8) M) depressed both the slope and maximal response of the control curve for vasopressin. Vasopressin produced further contractions in arterial rings with or without endothelium precontracted with prostaglandin F2 alpha or norepinephrine. In precontracted arterial rings and previously treated with the V1 vasopressinergic antagonist [(1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2- (O-methyl)-tyrosine-8-arginine)vasopressin] (10(-6) M) vasopressin caused endothelium-independent relaxation. The relaxation to vasopressin was reduced significantly by indomethacin (10(-6) M) and unaffected by the V1-V2 receptor antagonist [(1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2- (O-ethyl)-D-tyrosine-4-valine-8-arginine-9-desglycine)vasopressin] (10(-6) M) or by NG-monomethyl-L-arginine (10(-4) M).(ABSTRACT TRUNCATED AT 250 WORDS)