Vasopressin release does not contribute to pressor action of enkephalin in SHR.

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Abstract
The effects of injection of a peptidase-resistant analog of methionine-enkephalin, [D-ala2]-methionine-enkephalin, on blood pressure (BP), heart rate, and vasopressin release were studied in spontaneously hypertensive rats (SHR). Intravenous injection of [D-Ala2]-methionine-enkephalin (DAME) increased BP in both SHR and normotensive Wistar-Kyoto (WKY) controls, with a significantly greater increase in hypertensive rats. Intracerebroventricular injection of DAME produced a biphasic 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-(beta-mercapto-beta-beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine] arginine-vasopressin, did not block either component of the central enkephalin response in hypertensive rats. These date indicate that central enkephalin injection does not release vasopressin and that SHR are hyperresponsive to enkephalin. It is concluded that pressor systems other than that of vasopressin mediate the enkephalin-induced cardiovascular effects.