Training induces nonuniform increases in eNOS content along the coronary arterial tree

Abstract

Exercise training produces enhanced nitric oxide (NO)-dependent, endothelium-mediated vasodilator responses of porcine coronary arterioles but not conduit coronary arteries. The purpose of this study was to test the hypothesis that exercise training increases the amount of endothelial NO synthase (eNOS) in the coronary arterial microcirculation but not in the conduit coronary arteries. Miniature swine were either exercise trained or remained sedentary for 16--20 wk. Exercise-trained pigs exhibited increased skeletal muscle oxidative capacity, exercise tolerance, and heart weight-to-body weight ratios. Content of eNOS protein was determined with immunoblot analysis in conduit coronary arteries (2- to 3-mm ID), small arteries (301- to 1,000-microm ID), resistance arteries (151- to 300-microm ID), and three sizes of coronary arterioles [large (101- to 150-microm ID), intermediate (51- to 100-microm ID), and small (<50-microm ID)]. Immunoblots revealed increased eNOS protein in some sizes of coronary arteries and arterioles but not in others. Content of eNOS was increased by 60--80% in small and large arterioles, resistance arteries, and small arteries; was increased by 10--20% in intermediate-sized arterioles; and was not changed or decreased in conduit arteries. Immunohistochemistry revealed that eNOS was located in the endothelial cells in all sizes of coronary artery. We conclude that exercise training increases eNOS protein expression in a nonuniform manner throughout the coronary arterial tree. Regional differences in shear stress and intraluminal pressures during exercise training bouts may be responsible for the distribution of increased eNOS protein content in the coronary arterial tree.

Effects of Different Levels of Exercise Volume on Endothelium-Dependent Vasodilation: Roles of Nitric Oxide Synthase and Heme Oxygenase

“…We also found that high volume intens exercise led to hypertension and impairment of endothelium-dependent vascular relaxation, with marked and diffuse increases in eNOS and iNOS across three aortic layers. It is well recognized that NO participates in exerciseinduced enhancement of vascular function and remodeling (13,14,(19)(20)(21). In the present study, we also found a significant increase in aortic eNOS content after acute and chronic endurance training, in accordance with increased acetylcholine-induced vascular relaxation.…”

Rapid and Extensive Arterial Adaptations After Spinal Cord Injury

“…It may be possible that mechanisms and time course of vascular adaptations to deconditioning may differ between conduit (diameter) and resistance vessels (hyperemic flow response), as has been indicated previously in exercise-training studies in animals 26,27 and humans. 28 This hypothesis, however, needs further investigation.…”

Is Flow-Mediated Dilation Nitric Oxide Mediated?

“…For example, it is conceivable that different arteries possess distinct degrees of NO dependency. Previous studies have typically examined brachial or radial artery responses, making it somewhat difficult to extrapolate these findings to other conduit arteries, especially given the heterogeneity in endothelial NO synthase expression level 64 and vasodilator responsiveness 65 between different arterial beds. That said, the only extant femoral artery study demonstrated a significant effect of L-NMMA on the FMD response.…”