Role of Calcium-Sensitive K + Channels and Nitric Oxide in In Vivo Coronary Vasodilation From Enhanced Perfusion Pulsatility
- 2 January 2001
- journal article
- other
- Published by Wolters Kluwer Health in Circulation
- Vol. 103 (1) , 119-124
- https://doi.org/10.1161/01.cir.103.1.119
Abstract
Background—In vitro studies support K+Ca channel–induced smooth muscle hyperpolarization as underlying acetylcholine-mediated (or bradykinin-mediated) vasodilation that persists despite combined ni...Keywords
This publication has 31 references indexed in Scilit:
- Specificity of synergistic coronary flow enhancement by adenosine and pulsatile perfusion in the dogThe Journal of Physiology, 1999
- Substance P and bradykinin activate different types of KCa currents to hyperpolarize cultured porcine coronary artery endothelial cellsThe Journal of Physiology, 1999
- Enhanced acetylcholine and P2Y-receptor stimulated vascular EDHF-dilatation in congestive heart failureCardiovascular Research, 1999
- Sustained vessel dilation induced by increased pulsatile perfusion of porcine carotid arteries in vitroActa Physiologica Scandinavica, 1999
- The Alternative: EDHFJournal of Molecular and Cellular Cardiology, 1999
- ION CHANNELS IN VASCULAR ENDOTHELIUMAnnual Review of Physiology, 1997
- Transduction of physical force by the vascular wall: Role of phospholipase C and cytochrome P450 metabolites of arachidonic acidTrends in Cardiovascular Medicine, 1995
- Regulation of Arterial Tone by Activation of Calcium-Dependent Potassium ChannelsScience, 1992
- Both membrane stretch and fatty acids directly activate large conductance Ca2+‐activated K+ channels in vascular smooth muscle cellsFEBS Letters, 1992
- Shear stress-induced release of nitric oxide from endothelial cells grown on beads.Hypertension, 1991