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Am J Physiol Cell Physiol 259: C854-C861, 1990;
0363-6143/90 $5.00
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AJP - Cell Physiology, Vol 259, Issue 6 C854-C861, Copyright © 1990 by American Physiological Society


ARTICLES

Somatostatin increases voltage-dependent potassium currents in rat somatotrophs

C. Chen, J. Zhang, J. D. Vincent and J. M. Israel
Institute National de la Sante et de la Recherche Medicale U. 176, Bordeaux, France.

To study the modulatory effects of somatostatin on membrane K+ currents, whole cell voltage-clamp recordings were performed on identified rat somatotrophs in primary culture. In the presence of Co2+ (2 mM) and tetrodotoxin (1 microM) in the bath solution to block Ca2+ and Na+ inward currents, two types of voltage-activated K+ currents were identified on the basis of their kinetics and pharmacology. First, a delayed rectifier K+ current (IK) had a threshold of -20 mV, did not decay during voltage steps lasting 300 ms, and was markedly attenuated by extracellular application of tetraethylammonium (TEA, 10 mM). Second, a transient outward K+ current (IA) was activated at -40 mV (from a holding potential of -80 mV) and persisted despite the presence of TEA. This IA was blocked by 4-aminopyridine (2 mM). Somatostatin (10 nM) increased IK by 75% and IA by 45% without obvious effects on steady-state voltage dependency of activation or inactivation, and these effects were reversible. This increase in K+ currents may contribute in part to the inhibitory effect of somatostatin on growth hormone release.


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