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Endocrinology. 1997 Oct;138(10):4167-75.

Effects of K+ channel blockers on K+ channels, membrane potential, and aldosterone secretion in rat adrenal zona glomerulosa cells.

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Department of Biological Sciences, Northern Illinois University, DeKalb 60115, USA.


The hypothesis that angiotensin II (ANG II)-induced aldosterone secretion is mediated through inhibition of plasma membrane K+ channels was examined by measuring the effects of K+ channel blockers on K+ currents, membrane potential, and aldosterone secretion in rat adrenal glomerulosa cells. Effective K+ channel blockers were identified and studied using patch clamp methods on isolated glomerulosa cells in cell culture. Extracellular Cs+ (2-20 mm) caused a voltage-dependent inhibition of macroscopic K+ currents, exhibiting an apparent Kd of 2 mM for blockade of K+ current at membrane potentials near the K+ equilibrium potential. Outward K+ current opposed the Cs+ block, imparting a steep voltage dependence to this block. In single channel studies Cs blocked inward, but not outward, unitary currents through ANG II-regulated weakly voltage-dependent K+ channels, which are thought to control resting membrane potential. Cs+ reversibly depolarized the resting membrane potential at concentrations greater than or equal to the apparent Kd for K+ conductance inhibition (> or =2 mM). Depolarization consisted of a slow, maintained phase proportional to Cs+ concentration superimposed with 2- to 5-mV transient depolarizing events. Cs+ induced a Ca2+-dependent stimulation of aldosterone secretion in acutely dissociated cells, exhibiting an EC50 of approximately 3 mM. Maximal Cs+-induced secretion was quantitatively similar to 1 nM ANG II- or 8 mM K+-induced secretion. Cs+-induced secretion was not additive with that of ANG II. K+ channel blockers that did not inhibit weakly voltage-dependent K+ channels at rest (quinidine, apamin, and charybdotoxin) did not cause depolarization or stimulate aldosterone secretion. Furthermore, charybdotoxin did not significantly affect ANG II-induced aldosterone secretion, indicating that Ca2+-dependent maxi-K+ channels did not contribute to the control of aldosterone secretion in acutely dissociated cells. These data strongly support involvement of weakly voltage-dependent K+ channels in ANG II-induced aldosterone secretion, but also implicate roles for other channel classes in controlling membrane potential during ANG II-induced aldosterone secretion.

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