Vasopressin Release Does Not Contribute to Pressor Action of Enkephalin in SHR

SUMMARY The effects of Injection of a peptidase-reslstant analog of methionine-enkephalln, [D-Ala]- raethionine-eokephalln, on blood pressure (BP), heart rate, and vasopressin release were studied in spontaneously hypertensive rats (SHR). Intravenous injection of [D-AlaʼJ-roethlonlne-eflkephalln (DAME) Increased BP in both SHR and normotenslve Wlstar-Kyoto (WKY) controls, with a significantly greater increase in hypertenslre rats. Intracerebrorentrtcular injection of DAME produced a Diphasic increase in BP and an increase in heart rate in both groups. The initial pressor effect was significantly greater in the SHR. Plasma vasopressin levels in SHR were depressed relative to both untreated hypertensive rats and animals given vehicle control injections. Intravenous pretreatment with a vasopressin vasopressor antagonist, [l-(β- mercapto-β-β-cyclopentamethyleneproplonlc acid)$-(0-methyl)tyroslne] arglnine-vasopressin, did not block either component of the central enkephalin response in hypertensive rats. These data indicate that central enkephalin injection does not release vasopressin and that SHR are hyperresponslve to enkephalin. It is concluded that pressor systems other than that of vasopressin mediate the enkephalin-induced cardiovascular effects.