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AJP - Renal Physiology, Vol 258, Issue 3 473-F478, Copyright © 1990 by American Physiological Society
ARTICLES |
R. T. McCarthy, C. M. Isales, W. B. Bollag, H. Rasmussen and P. Q. Barrett
Miles Institute for Preclinical Pharmacology, West Haven, Connecticut 06516.
Atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone stimulated by any of these major physiological agonists: angiotensin II, adrenocorticotropic hormone, or K+. The stimulatory actions of each of these agonists depend on calcium influx through voltage-dependent calcium channels. Because two types of calcium channels have been previously described in bovine glomerulosa cells (T- and L-type), the patch-clamp technique was used to evaluate the effect of ANP on each voltage-dependent calcium channel type. ANP was found to differentially modulate these two channel types, stimulating L-current while inhibiting T-current. Inhibition of T-current resulted from a shift in the voltage dependence of inactivation to more negative potentials within the physiological range. These results indicate that the ANP-induced inhibition of aldosterone secretion may be partially mediated via a reduction of the calcium current through T-type channels.
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