Am J Physiol Cell Physiol AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 261: C218-C223, 1991;
0363-6143/91 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kato, M.
Right arrow Articles by Vincent, J. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kato, M.
Right arrow Articles by Vincent, J. D.

AJP - Cell Physiology, Vol 261, Issue 2 C218-C223, Copyright © 1991 by American Physiological Society


ARTICLES

Blockade by lithium ions of potassium channels in rat anterior pituitary cells

M. Kato, P. M. Lledo and J. D. Vincent
Laboratoire de Neurobiologie des Comportements, Institut National de la Sante, et de la Recherche Medicale Unite 176, Bordeaux, France.

Extracellular Li+ has been known to facilitate the basal secretion of growth hormone from anterior pituitary cells and of catecholamine from chromaffin cells. In both cases, the intracellular accumulation of Li+ seems to be the prerequisite, and the presence of extracellular Ca2+ is indispensable. In this series of experiments, we examined whether Li+ blocked K+ currents by using primary cultured anterior pituitary cells from male rats. K+ currents were measured in the whole cell configuration of the patch-clamp technique. Extracellular Li+ (140 mM) suppressed both the delayed rectifier K+ current (IK) and the transient outward K+ current to 71 and 69% of control, respectively, in a reversible manner. IK elicited by a voltage step to +70 mV from holding potential of -70 mV was suppressed by 32.5 mM internal Li+ to 28% of control. Half-maximal suppression of K+ conductance by internal Li+ was 16 mM. Furthermore, Ca(2+)-channel blocker methoxyverapamil potently suppressed Li(+)-induced growth hormone secretion. From these results we propose that the blockade by Li+ of K+ channels could depolarize the cells and activate Ca2+ channels, thereby promoting the influx of Ca2+ and hormone secretion as a mechanism of Li(+)-induced hormone secretion.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online