Role of Calcium-Sensitive K ⁺ Channels and Nitric Oxide in In Vivo Coronary Vasodilation From Enhanced Perfusion Pulsatility

Abstract

K(+)(Ca) activation and NO comodulate in vivo pulsatility-stimulated coronary flow, supporting an important role of a hyperpolarization pathway in enhanced mechanovascular signaling. Small- and intermediate-conductance K(+)(Ca) channels are the dominant species involved in modulating both pulse pressure- and bradykinin-induced in vivo coronary dilation.