Aldosterone-Induced Coronary Dysfunction in Transgenic Mice Involves the Calcium-Activated Potassium (BKCa) Channels of Vascular Smooth Muscle Cells
Author(s) -
Marie-Lory Ambroisine,
Julie Favre,
Patricia Oliviéro,
Camille Rodriguez,
Ji Gao,
Christian Thuillez,
JaneLise Samuel,
Vincent Richard,
Claude Delcayre
Publication year - 2007
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/circulationaha.107.722009
Subject(s) - iberiotoxin , medicine , endocrinology , apamin , aldosterone , myograph , charybdotoxin , vascular smooth muscle , aldosterone synthase , acetylcholine , potassium channel , vasodilation , chemistry , renin–angiotensin system , blood pressure , smooth muscle
Cardiomyocyte-specific overexpression of aldosterone synthase in male (MAS) mice induces a nitric oxide-independent coronary dysfunction. Because calcium-activated potassium (BKCa) channels are essential for vascular smooth muscle cell (VSMC) relaxation, we hypothesized that aldosterone alters their expression and/or function in VSMCs.
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