Vasopressin V(1) receptor-mediated activation of central sympatho-adrenomedullary outflow in rats.

The present study was designed to characterize the vasopressin receptor subtype involved in the vasopressin-induced activation of the central sympatho-adrenomedullary outflow using urethane-anesthetized rats. Intracerebroventricularly (i.c.v.) administered vasopressin (0.1, 0.2 and 0.5 nmol/animal) dose-dependently elevated plasma levels of adrenaline and noradrenaline (adrenaline>noradrenaline). The vasopressin (0.2 nmol/animal)-induced elevation of both catecholamines was significantly attenuated by [d(CH(2))(5)(1),Tyr(Me)(2),Arg(8)]-vasopressin, a selective vasopressin V(1) receptor antagonist, in a dose-dependent manner (0.1 and 0.2 nmol/animal, i.c.v.). The same doses (0.1 and 0.2 nmol/animal, i.c.v.) of [1-adamantaneacetyl(1),D-Tyr(Et)(2),Val(4),Abu(6), Arg(8,9)]-vasopressin, a potent vasopressin V(2) receptor antagonist, had no effect; however, a large dose of this antagonist (1.6 nmol/animal, i.c.v.) effectively reduced the vasopressin-induced elevation of catecholamines. On the other hand, [5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepine], a selective vasopressin V(2) receptor antagonist (5 and 10 nmol/animal, i.c.v.), had no effect on the vasopressin-induced elevation of catecholamines. The vasopressin-induced elevation of catecholamines was abolished by indomethacin, an inhibitor of cyclooxygenase (1.2 micromol/animal, i.c.v.). These results suggest that the vasopressin activates the central sympatho-adrenomedullary outflow by brain vasopressin V(1) receptor- and cyclooxygenase-dependent mechanisms in rats.