V2-like receptors mediate cerebral blood flow increase following vasopressin administration in rats.

Experiments were performed on anesthetized (chloral hydrate) Wistar rats to determine the effect of vasopressin (VP) on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), cerebrovascular resistance (CVR), and mean arterial blood pressure (MAP) before and after V1 or V2 VP receptor blockade. Influence of synthetic V2 receptor agonist (dVDAVP) on these variables was also tested. Intracarotid administration of 5 mU VP (Pitressin, n = 15) significantly increased CBF by 28% and CMRO2 by 27% and reduced CVR by 20% of control value. Intravenous (i.v.) infusion of dEt2AVP (V1 antagonist, 15 micrograms kg-1 h-1, n = 7) did not influence the effect of VP on CBF, CMRO2, and CVR but abolished MAP increase after VP. Intravenous (i.v.) infusion of d(CH2)5[D-Ile2,Abu4] AVP (V2 antagonist, 15 micrograms kg-1 h-1, n = 8) abolished the effect of VP on CBF, CMRO2, and CVR without changing its influence on MAP. Intracarotid administration of 12.5 ng dVDAVP (n = 7) increased CBF by 43% and CMRO2 by 29% and decreased CVR by 29% of control value. MAP was not affected. The results suggest that VP-induced CBF increase is, at least partly, caused by the rise of CMRO2 and mediated by V2-like receptors.