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High blood pressure and membrane depolarization down‐regulate Shaker ‐type K + channels in the rat cerebral circulation
Author(s) -
Joseph Biny K,
Tobin Ann A,
Rusch Nancy J
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1114
Subject(s) - cerebral arteries , depolarization , cerebral circulation , medicine , vascular smooth muscle , potassium channel , endocrinology , vasoconstriction , blot , blood pressure , membrane potential , chemistry , anatomy , microbiology and biotechnology , biology , biochemistry , smooth muscle , gene
A reduced expression of Shaker ‐type potassium (K v 1) channels in small cerebral arteries of spontaneously hypertensive rats (SHR) causes vasoconstriction, which may protect the distal blood brain barrier from barotrauma. The aims of this study were to: 1) determine if K v 1 channels also are down‐regulated in the cerebral circulation of aortic‐banded (Ao‐B) hypertensive rats, and 2) identify possible stimuli associated with hypertension that down‐regulate K v 1 channels. Cerebral arteries were micro‐dissected from Ao‐B hypertensive rats and sham‐operated rats. Western immunoblots showed a decreased expression in cerebral arteries of Ao‐B rats of three subunits that compose the Kv1 channels: the pore‐forming K v 1.2α and K v 1.5α subunits, and an ancillary K v 2β subunit. A rat cerebral vascular smooth muscle cell (VSMC) culture was developed to identify mechanisms that regulate K v 1 channel expression. Western blots verified that the cultured VSMCs expressed K v 1.2α, K v 1.5α and K v 2β subunits. When the cells were depolarized for 48 hours by 30 mmol/L KCl, a reduction in the expression levels of the K v 1 channel subunits was observed. These results suggest that: 1) a low expression of cerebrovascular K v 1 channels is a shared abnormality between cerebral arteries of SHR and hypertensive Ao‐B rats, and 2) membrane depolarization of VSMCs, an event associated with the myogenic response of arteries to high blood pressure, down‐regulates K v 1 channels in cerebral VSMCs. Supported by NIH 7R01HL059238‐08.