AJP - Endocrinology and Metabolism, Vol 256, Issue 2 E270-E276, Copyright © 1989 by American Physiological Society
Attenuation of the osmotic release of vasopressin by enkephalins in dogs
K. Matsui, T. Kimura, K. Ota, M. Shoji, M. Inoue, K. Iitake and K. Yoshinaga
Second Department of Internal Medicine Tohoku University School of Medicine, Sendai, Japan.
To assess the possible role of circulating enkephalins in the osmotic
release of vasopressin, Met5 (M-Enk)- or Leu5-enkephalin (L-Enk) dissolved
in 0.9 or 10% NaCl was infused to either anesthetized or conscious dogs at
a dose of 3.5 nM.kg-1.min-1 for 15 min. Intravenous infusion of M-Enk or
L-Enk produced 150- to 200-fold increases in their plasma levels, and the
elevated levels were maintained during the infusion. Although blood
pressure (BP) in anesthetized dogs decreased significantly during L-Enk
infusion, BP in conscious dogs was unaffected by both enkephalins. Neither
M-Enk nor L-Enk infusion affected plasma vasopressin concentration (PAVP)
in these anesthetized and conscious dogs that were not osmotically
stimulated. PAVP in conscious time control dogs increased significantly
after start of 10% NaCl infusion in spite of an increase in BP. M-Enk or
L-Enk significantly blunted the increase in PAVP induced by 10% NaCl
infusion. This attenuation was not accompanied by any significant changes
in plasma sodium concentration and BP compared with those of time control
dogs. Thus increase in plasma enkephalins attenuates the osmotic release of
vasopressin.
