Vasopressin-induced contraction in the rat basilar artery in vitro

Vasopressin ([Arg(8)]vasopressin)-induced contraction was characterized using receptor agonists and antagonists for vasopressin and channel blockers in the rat basilar artery ring preparations. Vasopressin induced rhythmic contractions superimposed on a contraction in endothelium-intact preparations but not in denuded ones. Endothelium removal shifted the concentration-response curve for vasopressin leftward and upward. In endothelium-denuded preparations, vasopressin V-1 receptor antagonist shifted the concentration-response curve for vasopressin downward and rightward. Vasopressin V-1 receptor agonist caused contraction but V-2 receptor agonist did not. The contractile response to vasopressin was partly inhibited by nifedipine, SK&F 96365 (l-[beta-[3-(4-methoxyphenyl)propoxy]-4-metho- xyphenethyl]-1 H-imidazole) and niflumic acid. In the absence of extracellular Ca2+, vasopressin produced a transient contraction. Charybdotoxin produced an upward and leftward shift of the concentration-response curve for vasopressin. These results suggest that vasopressin elicits contraction due to Ca2+ influx through voltage-dependent and receptor-operated Ca2+ channels and to Ca2+ release from Ca2+ stores by activating vasopressin V-1 receptors in the rat basilar artery. (C) 2001 Elsevier Science B.V. All rights reserved.