Specific activation of KCa channels contribute to Omega 3 fatty acid ‐Induced Pulmonary Vasodilation

Background Pulmonary hypertension (PH) is a progressive and fatal cardiovascular disorder and characterized by a sustained elevation of pulmonary artery pressure. Loss of endogenous vasodilatory factors in the pulmonary artery is one of main contributing factor of PH. Omega 3 fatty acid (DHA), which has been shown to have many beneficial effects on the cardiovascular system. But its regulatory effect on pulmonary vascular tone and pressure is largely unknown. Methods: we investigated the role of DHA and its effect on the pulmonary circulation. the whole‐cell patch‐clamp technique was to study the potassium (K+) current in primary human Pulmonary Artery Smooth muscle cells (hPASMCs). Wire myograph was used to study the pulmonary vascular tone. Isolated, perfused and ventilated mouse lungs system was used for recording pulmonary artery pressure (PAP). RESULTS: DHA dose dependently activates the whole cell K+ current in primary hPASMCs. The activated current was significantly inhibited with treatment of Iberiotoxin, but application of 4‐Aminopyridine did not have any effect on the activated current. Suggesting, DHA Preferential activates Kca channels over KV channels in hPASMCs. In preconstricted mouse pulmonary artery, DHA cause a vasodilation. To depict the role of DHA in ex‐vivo model of pulmonary artery pressure, we used isolated perfused mouse lungs in the presence of U‐46619,where DHA showed a pronounced decrease in mean PAPConclusion Our findings indicate that DHA, Preferential activates KCa channels in hPAVSMCs, and leading to pulmonary vasorelaxation. This benifical effects of DHA as potential vasodilatory, might therapeutic option in PH