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Endocrinology, Vol 124, 1094-1096, Copyright © 1989 by Endocrine Society
ARTICLES |
J Wang, KG Baimbridge and PC Leung
Department of Obstetrics and Gynecology, University of British Columbia, Grace Hospital, Vancouver, Canada.
A physiological role of angiotensin II (Ang II) on the ovary has been suggested recently, but the mechanism of action is not understood. In 18 out of 44 individual rat granulosa cells loaded with fura-2, Ang II caused a rapid and transient increase in intracellular free calcium ion concentration, [Ca2+]i. In 12 of these cells, 10(-5) M Ang II caused a 3.7 +/- 0.5-fold increase in [Ca2+]i. After 74 +/- 4 sec, [Ca2+]i returned to the resting levels (96.0 +/- 3.7 nM). Angiotensin I was without effect (n = 9). The effect of Ang II on [Ca2+]i changes could be completely blocked by a potent long-acting Ang II antagonist, [Sar1, Thr8]-angiotensin II, suggesting a receptor-mediated mechanism. The present results strongly indicate that rapid alterations in [Ca2+]i is an early step in the signal transduction of Ang II in a subpopulation of cells in the rat ovary.
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