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1 Department of Pharmacology, The University of Vermont College of Medicine, Burlington, Vermont 05405; and 2 Medical Biotechnology Center, University of Maryland Biotechnology Institute, Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201
Elevated intracellular Ca2+ ([Ca2+]i) has been implicated in contractile and phenotypic changes in arterial smooth muscle during hypertension. This study examined the role of membrane potential and [Ca2+]i in altered gene expression in cerebral arteries of a rat (Dahl) genetic model of salt-sensitive hypertension. Cerebral arteries from hypertensive animals (Dahl salt-sensitive) exhibited a tonic membrane depolarization of ~15 mV compared with normotensive (Dahl salt-resistant) animals. Consistent with this membrane depolarization, voltage-dependent K+ currents were decreased in cerebral artery myocytes isolated from hypertensive animals. Arterial wall Ca2+ was elevated in cerebral arteries from hypertensive animals, an effect reversed by diltiazem, a blocker of voltage-dependent Ca2+ channels. This depolarization-induced increase in [Ca2+]i was associated with increased activation of the transcription factor, cAMP response element binding protein, and increased expression of the immediate early gene c-fos, both of which are reversed by acute exposure to the voltage-dependent Ca2+ channel blocker nisoldipine. This study provides the first information linking altered Ca2+ handling to changes in gene expression in cerebral arteries during hypertension.
cerebral arteries; calcium; potassium channels; hypertension
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