Potential Roles of Exercise in Regulating Myoendothelial Feedback in Resistance Arteries

초록

PURPOSE Resistance arteries rely on tightly coordinated signaling between vascular smooth muscle cells (SMCs) and endothelial cells (ECs) to regulate vascular tone and ensure appropriate tissue perfusion. Myoendothelial feedback via gap junctions is crucial in limiting excessive vasoconstriction triggered by myogenic and sympathetic stimuli. This review synthesizes current knowledge on second messenger-dependent SMC-to-EC communication and explores how exercise training modulates these heterocellular signaling pathways to influence myoendothelial feedback. METHODS Relevant literature was systematically retrieved from major scientific databases (e.g., PubMed and Web of Science), with a primary focus on studies examining vascular myoendothelial feedback regulation and the effect of exercise training on SMC-EC heterocellular communication. RESULTS SMC activation by adrenergic or purinergic stimuli generates intracellular Ca2+ and IP3 signals that are transmitted to adjacent ECs via myoendothelial gap junctions. These signals elicit localized endothelial Ca2+ events, stimulate nitric oxide production, activate endothelial IKCa and SKCa channels, and induce endothelium-dependent hyperpolarization, collectively suppressing SMC contraction. Ca2+ diffusion and IP3 transfer contribute to this negative feedback, with growing evidence supporting C2+/IP3-dependent signaling as a dominant mechanism during physiological sympathetic activation. Exercise training enhances endothelial C2+ signaling capacity, improves gap junctional communication, and augments downstream vasodilatory responses. CONCLUSIONS Myoendothelial feedback represents a critical protective mechanism against excessive vasoconstriction in resistance arteries. Exercise training reinforces this negative feedback by strengthening endothelial signaling and heterocellular communication, thereby promoting vascular homeostasis during physiological stress.

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