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AJP - Endocrinology and Metabolism, Vol 258, Issue 4 E555-E561, Copyright © 1990 by American Physiological Society
ARTICLES |
A. Spat, I. Balla, T. Balla, P. Enyedi, G. Hajnoczky and T. Rohacs
Department of Physiology, Semmelweis University Medical School, Budapest, Hungary.
Angiotensin-induced aldosterone production by superfused adrenal glomerulosa cells was potentiated by Ni2+ (0.1 mM), added either at the onset of stimulation with angiotensin II or 1 h later. Nickel did not influence the effect of adrenocorticotropic hormone or potassium on aldosterone production. Nickel failed to modify angiotensin-induced changes in phospholipid metabolism or the formation of inositol phosphates and slightly reduced the enhancement of 45Ca influx. Uptake of Ni2+ into glomerulosa cells was increased by depolarization in a dihydropyridine-insensitive manner. Because nickel selectively potentiates the sustained phase of the response to a calcium-mobilizing hormone, it may serve as a suitable tool in elucidating the signal transduction process during the sustained phase of stimulation.
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