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Am J Physiol Lung Cell Mol Physiol 277: L662-L666, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 3, L662-L666, September 1999

RAPID COMMUNICATION
Dexfenfluramine increases pulmonary artery smooth muscle intracellular Ca2+, independent of membrane potential

Helen L. Reeve1,2, Stephen L. Archer3, Marjorie Soper1, and E. Kenneth Weir1,4

Departments of 1 Medicine and 2 Physiology, University of Minnesota, Minneapolis 55455; 4 Department of Medicine, Veterans Affairs Medical Center, Minneapolis, Minnesota 55417; and 3 Departments of Medicine and Physiology, University of Alberta, Edmonton, Canada T6G 267

The anorexic agent dexfenfluramine causes the development of primary pulmonary hypertension in susceptible patients by an unknown mechanism that may include changes in K+-channel activity and intracellular Ca2+ concentration ([Ca2+]i). We investigated the dose-dependent effects of dexfenfluramine on [Ca2+]i, K+ current, and membrane potential in freshly dispersed rat pulmonary artery smooth muscle cells. Dexfenfluramine caused a dose-dependent (1-1,000 µM) increase in [Ca2+]i, even at concentrations lower than those necessary to inhibit K+ currents (10 µM) and cause membrane depolarization (100 µM). The [Ca2+]i response to 1 and 10 µM dexfenfluramine was completely abolished by pretreatment of the cells with 0.1 µM thapsigargin, whereas the response to 100 µM dexfenfluramine was reduced. CoCl2 (1 mM), removal of extracellular Ca2+, and pretreatment with caffeine (1 mM) reduced but did not abolish the response to 100 µM dexfenfluramine. We conclude that dexfenfluramine increases [Ca2+]i in rat pulmonary artery smooth muscle cells by both release of Ca2+ from the sarcoplasmic reticulum and influx of extracellular Ca2+.

intracellular calcium; potassium channels; sarcoplasmic reticulum; anorexics


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