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Effects of [Sar 1 ] Angiotensin II on Proenkephalin Gene Expression and Secretion of [Met 5 ]Enkephalin in Bovine Adrenal Medullary Chromaffin Cells
Author(s) -
Suh Harold H.,
Mar EngChun,
Hudson Pearlie M.,
McMillian Michael K.,
Hong JauShyong
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb08340.x
Subject(s) - endocrinology , medicine , angiotensin ii , losartan , saralasin , stimulation , chemistry , receptor , chromaffin cell , enkephalin , biology , adrenal medulla , catecholamine , opioid
We have studied the effect of [Sar 1 ]angiotensin II [S 1 ‐AII; a degradation‐resistant analogue of angiotensin II (All)] on the release of [Met 5 ]enkephalin (ME) and proenkephalin A (proENK) gene expression. Short‐term (15‐min to 1‐h) stimulation of bovine adrenal medullary chromaffin (BAMC) cells with S 1 ‐AII at concentrations from 0.1 to 100 n M had no significant effect on secretion of ME, whereas high concentrations of S 1 ‐AII (3 to 100 μM ) produced a concentration‐dependent increase in the concentration of ME in the incubation media. In contrast, long‐term (3‐ to 24‐h) stimulation with low concentrations (0.1 n M‐1 μM ) of S 1 ‐AII increased the secretion of ME in a concentration‐dependent manner (EC 50 = 1 nM ). The intracellular level of ME was not changed by long‐term treatment with S 1 ‐AII (100 nM ). In addition to increased ME secretion, long‐term (24‐h) stimulation with S 1 ‐AII increased the expression of proENK mRNA in a concentration‐dependent manner (EC 50 = 4 n M ). Losartan (2‐n‐butyl‐4 chloro‐5‐hydroxy‐methyl‐l‐[(2′‐(l H ‐tetrazol‐5‐yl)biphenyl‐4‐yl)‐meth‐yl]imidazole potassium salt, a type 1 All receptor antagonist inhibited these effects, whereas PD123319 (50 μM , a type 2 All receptor antagonist) was inactive. Our results suggest that All in BAMC cells exerts a major effect on the long‐term regulation of expression of proENK mRNA and secretion of ME. These effects appear to be mediated by type 1‐like All receptors.