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Abstract

Ionic and secretory response of pancreatic islet cells to minoxidil sulfate.

M H Antoine, M Hermann, A Herchuelz and P Lebrun
Journal of Pharmacology and Experimental Therapeutics July 1991, 258 (1) 286-291;
M H Antoine
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M Hermann
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A Herchuelz
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P Lebrun
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Abstract

Minoxidil sulfate is an antihypertensive agent belonging to the new class of vasodilators, the "K+ channel openers." The present study was undertaken to characterize the effects of minoxidil sulfate on ionic and secretory events in rat pancreatic islets. The drug unexpectedly provoked a concentration-dependent decrease in 86Rb outflow. This inhibitory effect was reduced in a concentration-dependent manner by glucose and tolbutamide. Minoxidil sulfate did not affect 45Ca outflow from islets perfused in the presence of extracellular Ca++ and absence or presence of glucose. However, in islets exposed to a medium deprived of extracellular Ca++, the drug provoked a rise in 45Ca outflow. Whether in the absence or presence of extracellular Ca++, minoxidil sulfate increased the cytosolic free Ca++ concentration of islet cells. Lastly, minoxidil sulfate increased the release of insulin from glucose-stimulated pancreatic islets. These results suggest that minoxidil sulfate reduces the activity of the ATP-sensitive K+ channels and promotes an intracellular translocation of Ca++. The latter change might account for the effect of the drug on the insulin-releasing process. However, the secretory response to minoxidil sulfate could also be mediated, at least in part, by a modest Ca++ entry.

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Journal of Pharmacology and Experimental Therapeutics
Vol. 258, Issue 1
1 Jul 1991
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Abstract

Ionic and secretory response of pancreatic islet cells to minoxidil sulfate.

M H Antoine, M Hermann, A Herchuelz and P Lebrun
Journal of Pharmacology and Experimental Therapeutics July 1, 1991, 258 (1) 286-291;

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Abstract

Ionic and secretory response of pancreatic islet cells to minoxidil sulfate.

M H Antoine, M Hermann, A Herchuelz and P Lebrun
Journal of Pharmacology and Experimental Therapeutics July 1, 1991, 258 (1) 286-291;
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