Exercise training reinforces myoendothelial negative feedback against excessive vasoconstriction by strengthening endothelial Ca2+ signaling and heterocellular communication.
Does exercise training improve myoendothelial feedback in resistance arteries?
Exercise training reinforces myoendothelial negative feedback by strengthening endothelial signaling and heterocellular communication, promoting vascular homeostasis during physiological stress.
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 Ca 2+ and IP3 signals that are transmitted to adjacent ECs via myoendothelial gap junctions.These signals elicit localized endothelial Ca 2+ events, stimulate nitric oxide production, activate endothelial IKCa and SKCa channels, and induce endothelium-dependent hyperpolarization, collectively suppressing SMC contraction.Ca 2+ diffusion and IP3 transfer contribute to this negative feedback, with growing evidence supporting C 2+ +/IP3-dependent signaling as a dominant mechanism during physiological sympathetic activation.Exercise training enhances endothelial C 2+ 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.
Park et al. (Thu,) conducted a review in Vascular homeostasis and myoendothelial feedback regulation. Exercise training was evaluated. Exercise training reinforces myoendothelial negative feedback against excessive vasoconstriction by strengthening endothelial Ca2+ signaling and heterocellular communication.