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Am J Physiol Lung Cell Mol Physiol 274: L186-L195, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 2, L186-L195, February 1998

Effect of dehydroepiandrosterone on hypoxic pulmonary vasoconstriction: a Ca2+-activated K+-channel opener

Imad S. Farrukh, Wei Peng, Urszula Orlinska, and John R. Hoidal

Division of Respiratory, Critical Care and Occupational Medicine, Department of Internal Medicine, The University of Utah Health Science Center, Salt Lake City 84132; and Pharmadigm, Inc., Salt Lake City, Utah 84109

In the present study, we investigated the effects of the naturally occurring hormone dehydroepiandrosterone (DHEA) on hypoxic pulmonary vasoconstriction (HPVC) in isolated ferret lungs and on K+ currents in isolated and cultured ferret pulmonary arterial smooth muscle cells (FPSMCs). Severe alveolar hypoxia (3% O2-5% CO2-92% N2) caused an initial increase in pulmonary arterial pressure (Ppa) that was followed by a reversal in pulmonary hypertension. Maintaining alveolar hypoxia caused a sustained secondary increase in Ppa. Pretreating the lungs with the K+-channel inhibitor tetraethylammonium (TEA) caused a small increase in baseline Ppa, potentiated HPVC, and prevented the reversal of HPVC during the sustained alveolar hypoxia. Treating the lungs with DHEA caused a near-complete reversal of HPVC in control lungs and in lungs that were pretreated with TEA. DHEA also reversed the KCl-induced increase in Ppa. In FPSMCs, DHEA caused an adenosine 3',5'-cyclic monophosphate- and guanosine 3',5'-cyclic monophosphate-independent increase in activity of the Ca2+-activated K+ (KCa) current. In a cell-attached configuration, DHEA caused a mean shift of -22 mV in the voltage-dependent activation of the KCa channel. We conclude that DHEA is a novel KCa-channel opener of the pulmonary vasculature.

pulmonary circulation; pulmonary hypertension; calcium-activated potassium-channel agonist; potassium-channel opener; potassium currents; tetraethylammonium


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