Contractile effects of perivascularly applied vasopressin on the pial artery of the cat brain.

1. The effects of perivascularly applied vasopressin on the diameter of pial arteries (control 298 +/- 14 S.E. micron) of the brain were examined after chronic implantation of a cranial window in fifteen anaesthetized cats. 2. Application of vasopressin resulted in a dose-dependent contraction. The threshold concentration for contraction was 3 X 10(-10) M, the half-maximal effective concentration (ED50) (1.6 +/- 0.2) X 10(-9) M, and the maximum reduction in artery diameter 37 +/- 2%. 3. The contraction was powerfully inhibited by perivascular application of a 10(-7) M solution of the vasopressin antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin. 4. Perivascular application of noradrenaline induced a dose-dependent contraction of the pial artery. The ED50 was (8.9 +/- 2.5) X 10(-7) M, and the maximum reduction in artery diameter was 33 +/- 2%. 5. Such noradrenaline-induced contraction was not modified at all in the presence of a subthreshold dose (2 X 10(-10) M) of vasopressin (P greater than 0.05, for the over-all difference in size of the contraction, ED50 and maximum contraction). 6. In another experimental setting it was also found that neither the subthreshold nor a suprathreshold (10(-9) M) dose of vasopressin modified the contraction induced by 10(-6) M-noradrenaline (P greater than 0.05, compared to the contraction in the absence of vasopressin). 7. Thus a powerful and sensitive contractile response of the pial arteries to perivascularly applied vasopressin was demonstrated. However, the modifying effect of vasopressin on the contraction induced by perivascularly applied noradrenaline was minimal.