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AJP - Endocrinology and Metabolism, Vol 263, Issue 4 E760-E765, Copyright © 1992 by American Physiological Society
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M. V. Kanazirska, P. M. Vassilev, S. J. Quinn, D. L. Tillotson and G. H. Williams
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
The effects of angiotensin II (ANG II) on single K+ channels were studied in rat and bovine adrenal zona glomerulosa (ZG) cells, using the patch-clamp technique. ANG II (0.1-10 nM) induced substantial inhibition of inward rectifier and delayed rectifier K+ channel activities in rat and bovine ZG cells. Analysis of single-channel activities showed that the ANG II-induced channel-blocking effect involved reductions in the probability of the open state (Po) and the mean open time. The changes in these channel parameters occurred at all test voltages, indicating that the effect of ANG II was voltage independent. ANG II could not interact directly with the extracellular sides of the membranes in these experiments using cell-attached patches. Therefore, the effect of ANG II on K+ channels must occur through an indirect cytosolic transduction pathway. The ANG II-induced block of K+ channels will result in membrane depolarization, which may activate voltage-dependent Ca2+ channels, thereby increasing cytosolic free Ca2+ and stimulating aldosterone secretion. These channel-modulating actions of ANG II may be an important step in the initial sequence of events underlying its transduction mechanism.
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X.-L. Chen, D. A. Bayliss, R. J. Fern, and P. Q. Barrett A role for T-type Ca2+ channels in the synergistic control of aldosterone production by ANG II and K+ Am J Physiol Renal Physiol, May 1, 1999; 276(5): F674 - F683. [Abstract] [Full Text] [PDF] |
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