Effect of Hypoxia-Reoxygenation on Endothelial Function in Porcine Cardiac Microveins

Role of Large-conductance Calcium-activated Potassium Channels of Coronary Arteries in Heart Preservation

“…24,25 Most studies on the effect of hypoxia on BK Ca were conducted in pulmonary arteries. 26,27 Because our previous studies suggested that H-R impairs EDHF-mediated relaxation in both coronary microarteries and cardiac veins, 18,19,28,29 in the present study we investigated the effect of ischemia on the EDHF-targeting channels in VSMC BK Ca , by using the patch-clamp technique and isometric force measurement.…”

“…The complete details of normalization have been described previously. [14][15][16]18,19 Pre-contraction and relaxation. The vessels were either pre-contracted with U 46619 (Ϫ8.4 to Ϫ7 logM) or high K ϩ (20 to 30 mmol/liter) solution.…”

“…The full details have been described previously. 18,19 Normalization procedure for small coronary arteries. All rings were equilibrated at 37 Ϯ 0.1°C for 45 minutes before and after normalization.…”

“…[12][13][14][15][16][17] Accordingly, our previous studies have shown that exposure to hypoxia significantly reduces bradykinin-induced relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) in both coronary microarteries and cardiac veins. 18,19 Calcium-activated potassium channels (K Ca ) have several subtypes. The large-conductance K Ca (BK Ca ) are the predominant type of K Ca in VSMCs, presenting high levels of single-channel conductance (between 100 and 300 pS) and strongly affecting the membrane potential and the contractility/relaxation of arteries, particularly in the coronary arteries.…”

Intracellular pH in the Resistance Vasculature: Regulation and Functional Implications

“…As such, hypoxia-reoxygenation causes myocardial damage, which can be reduced by prior inhibition of Na + /H + exchange [115,116,117]. Similarly, endothelial dysfunction can be caused by hypoxia-reoxygenation [118,119,120] and beneficial effects of specific Na + /H + exchange inhibitors have been suggested [120,121]. While these findings support that Na + /H + exchange is involved in the pathogenesis of ischemic cell injury, the relative contribution of Na + /H + exchange inhibition in cardiomyocytes, ECs and potentially other cell types to alleviate development of myocardial dysfunction still requires further investigation.…”