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Caveolin‐1 ablation induces functional K Ca channel activation and attenuates the myogenic response in cerebral arteries
Author(s) -
Adebiyi Adebowale,
Zhao Guiling,
Cheranov Sergey Y,
Ahmed Abu,
Jaggar Jonathan H
Publication year - 2007
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.21.5.a521
Subject(s) - myogenic contraction , cerebral arteries , iberiotoxin , vasoconstriction , medicine , caveolae , myocyte , constriction , chemistry , cardiology , anatomy , endocrinology , vasodilation , signal transduction , biochemistry , smooth muscle
Intravascular pressure‐induced vasoconstriction (the “myogenic response”) is intrinsic to arterial myocytes, but mechanisms that underlie this response are unresolved. Here, we investigated the physiological function of caveolin‐1, a protein required for arterial myocyte caveolae formation, in mediating the cerebral artery myogenic response. Pressure‐induced changes in arterial wall membrane potential, intracellular calcium concentration ([Ca 2+ ] i ), and myogenic tone were attenuated in cerebral arteries from cav‐1 deficient (cav‐1 −/− ) mice, when compared with arteries from control (cav‐1 +/+ ) mice. Although 60 mM K + induced a smaller [Ca 2+ ] i elevation and constriction in cav‐1 −/− arteries, extracellular Ca 2+ removal and diltiazem, an L‐type Ca 2+ channel blocker, similarly dilated cav‐1 +/+ and cav‐1 −/− arteries. Iberiotoxin, a selective K Ca channel blocker, induced a similar depolarization and constriction in pressurized cav‐1 +/+ and cav‐1 −/− arteries. However, total K Ca channel protein was similar in cav‐1 +/+ and cav‐1 −/− arteries. Given that the hyperpolarized membrane potential of cav‐1 −/− arteries would reduce K Ca channel current, these data suggest that K Ca channel activity is elevated in cav‐1 −/− arteries and may contribute to the attenuated myogenic constriction. In summary, data indicate that cav‐1 expression is required for a full cerebral artery myogenic response.