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MECHANISMS FOR REGULATION OF ARTERIAL TONE BY Ca 2+ ‐ DEPENDENT K + CHANNELS IN HYPERTENSION
Author(s) -
Rusch Nancy J.,
Liu Yanping,
Pleyte Kay A.
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb01173.x
Subject(s) - membrane potential , medicine , membrane , mesenteric arteries , chemistry , blood pressure , vascular smooth muscle , biophysics , patch clamp , homeostasis , endocrinology , anatomy , artery , smooth muscle , electrophysiology , biology , biochemistry
SUMMARY 1. The membrane potential and reactivity of arterial smooth muscle cells is regulated by a variety of K + channels, which are highly expressed in vascular smooth muscle meuscle membrances. 2. Of these K + channel types, the high‐conductance, Ca 2+ ‐ependent K + channel appears to be up‐regulated in arterial smooth muscle membrances from hypertensive animals. 3. Patch‐clamp studies show that whole‐cell membrances and membrane patches of arterial smooth muscle obtained from rats with genetic or renal hypertension show an increased macroscopic and single‐channel Ca 2+ ‐activated K + current. Pharmacological block of this K + current profoundly constricts aortic, renal, mesenteric and femoral arteries obtained from the same hypertensive animals, suggesting that Ca 2+ ‐dependent K + current is a critical determinant of resting membrane potential in arterial muscle exposed to elevated blood pressure. 4. Thus, K + efflux through Ca 2+ ‐dependent K + channels appears to constitute an important homeostatic mechanism for buffering increases in arterial reactivity in hypertension.