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Regular aerobic exercise (RAEX) elicits several positive adaptations in all organs and tissues of the body, culminating in improved health and well-being. Indeed, in over half a century, many studies have shown the benefit of RAEX on cardiovascular outcome in terms of morbidity and mortality. RAEX elicits a wide range of functional and structural adaptations in the heart and its coronary circulation, all of which are to maintain optimal myocardial oxygen and nutritional supply during increased demand. Although there is no evidence suggesting that oxidative metabolism is limited by coronary blood flow (CBF) rate in the normal heart even during maximal exercise, increased CBF and capillary exchange capacities have been reported. Adaptations of coronary macro- and microvessels include outward remodelling of epicardial coronary arteries, increased coronary arteriolar size and density, and increased capillary surface area. In addition, there are adjustments in the neural and endothelial regulation of coronary macrovascular tone. Similarly, there are several adaptations at the level of microcirculation, including enhanced (such as nitric oxide mediated) smooth muscle-dependent pressure-induced myogenic constriction and upregulated endothelium-dependent/shear-stress-induced dilation, increasing the range of diameter change. Alterations in the signalling interaction between coronary vessels and cardiac metabolism have also been described. At the molecular and cellular level, ion channels are key players in the local coronary vascular adaptations to RAEX, with enhanced activation of influx of Ca2+ contributing to the increased myogenic tone (via voltage-gated Ca2+ channels) as well as the enhanced endothelium-dependent dilation (via TRPV4 channels). Finally, RAEX elicits a number of beneficial effects on several haemorheological variables that may further improve CBF and myocardial oxygen delivery and nutrient exchange in the microcirculation by stabilizing and extending the range and further optimizing the regulation of myocardial blood flow during exercise. These adaptations also act to prevent and/or delay the development of coronary and cardiac diseases. [ABSTRACT FROM AUTHOR]

The role of acetylcholine (ACh) in the release of vasodilators and constrictors from the venular endothelium was analyzed in isolated pressure- and norepinephrine (NE)-constricted rodent gracilis muscle venules. Administration of ACh in isolated NE-constricted rat gracilis muscles induced skeletal muscle dilation and constriction. Furthermore, the vascular effects of ACh were mediated by dilator and constrictor factors such as nitric oxide and prostaglandin H2.

The role of epinephrine and endothelium in pressure-sensitive myogenic response in skeletal muscle venules were investigated using first-order venules of rat gracilis muscle. The venules showed increases in diameter in response to perfusion pressure (PP). In passive conditions, the pressure-diameter curve shifted upwards, but shifted downwards in the presence of norepinephrine (NE). The removal of endothelium caused a marked decrease in venular diameters. These results suggest that NE is involved in the regulation of myogenic tone in rat skeletal muscle.

A study was conducted to assess the consequence of axial stretch on vascular smooth muscle (VSM) transmembrane potential and external diameter on intact and deendothelialized rat saphenous veins (SV). The results reveal that the axial stretch of SV can result in the liberation of factors derived from endothelium that hyperpolarize venous VSM and attenuate stretch induced and adrenergic vasoconstriction.

Presents a study which investigated the effects of increases in perfusate flowing shear stress on the diameter of isolated venules of gracilis muscle of rats. Methodology; Factors responsible for the mediation of responses; Findings of the study.

Examines the endothelium-derived factors involved in the mediation of response of rat gracilis muscle venules to acetylcholine and other vasoactive agents. Role of veins and venules in the body; Effect of chemicals released from the venular endothelium on the arteriolar resistance.