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AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 1 87-R93, Copyright © 1991 by American Physiological Society
ARTICLES |
K. T. Sato, K. Saga, M. Ohtsuyama, T. Takemura, W. H. Kang, F. Sato, Y. Suzuki and K. Sato
Department of Dermatology, University of Iowa College of Medicine, Iowa City 52242.
The ionic mechanism of beta-adrenergic sweating is unknown. In isolated rhesus eccrine secretory coils, K efflux was determined by an extracellular K electrode and cellular monovalent ions by X-ray microanalysis. Isoproterenol (Iso) induced a small (dose-dependent propranolol-inhibitable) K efflux followed by net K reuptake. Similar K response was seen with forskolin, theophylline, or isobutyl-methylxanthine (IBMX). The net K uptake often exceeded the net K efflux, causing a small net accumulation of K. Bumetanide (BT) and ouabain not only abolished the Iso (with or without IBMX) -induced net K uptake but increased the Iso-induced initial K efflux about threefold. BT and ouabain drastically decreased K and Cl concentrations in the clear cell (by X-ray microanalysis) only in the presence of Iso plus IBMX, suggesting that adenosine 3',5'-cyclic monophosphate (cAMP) may simultaneously stimulate both KCl efflux (by unknown mechanisms) and K reuptake (presumably by BT-sensitive cotransporters and ouabain-sensitive Na pumps). Thus the cAMP-mediated ion movement is different from the cholinergic mechanism that is characterized by the net KCl loss, cell shrinkage (Saga et al., J. Membr. Biol. 107: 13-24, 1989; Takemura et al., J. Membr. Biol. In press), and no augmentation of methacholine-induced K efflux by BT or ouabain.
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