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Coronary Arteriolar Dilation to Acidosis
Author(s) -
Hiroshi Ishizaka,
Siva R. P. Gudi,
John A. Frangos,
Lih Kuo
Publication year - 1999
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.99.4.558
Subject(s) - vasodilation , medicine , acidosis , glibenclamide , potassium channel , arteriole , pharmacology , nitric oxide , vasoconstriction , endocrinology , cardiology , anesthesia , microcirculation , diabetes mellitus
We previously demonstrated that coronary arteriolar dilation in response to acidosis is mediated by the opening of ATP-sensitive potassium (KATP) channels. However, the signal transduction involved in the KATP-channel activation during acidosis has not been elucidated. A recent study in cardiac myocytes implied that pertussis toxin (PTX)-sensitive G proteins may be involved in the signal transduction for KATP-channel activation. However, it remains unclear whether this transduction process also occurs in the vascular tissue and, in particular, whether it exerts functional dilation in response to acidosis.

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