Exercise training and responsiveness of isolated coronary arteries

Rogers, Paul J.; Miller, Trey; Bauer, Brent A.; Brum, José M.; Bové, Alfred A.; Vanhoutte, Paul M.

doi:10.1152/jappl.1991.71.6.2346

Cited by 48 publications

(33 citation statements)

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“…A similar finding using noradrenaline and KC1 was reported in exercise training ofYucatan miniature swine (Oltman et al, 1992). In the dog, however, Rogers et al (1991) demonstrated that contractile responses of the endothelium-intact epicardial coronary arteries (rings) to noradrenaline and phenylephrine were not different between exercised and sedentary control dogs. In exercise trained rats (both running and swimming) Edwards et al (1985) reported no changes in contractile responses to noradrenaline of endothelium-intact thoracic helical strips between those obtained from exercise trained and sedentary control rats.…”

Section: Discussionsupporting

confidence: 83%

Effect of swimming on vascular reactivity to phenylephrine and KC1 in male rats

Jansakul

1995

British J Pharmacology

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1 The present study aimed to examine whether there is any change in vascular responsiveness to phenylephrine and KCl during exercise, and whether the vascular endothelium plays a role in these changes. 2 Adult male rats were subjected to a swimming schedule every day for 5-6 weeks. Studies were performed in vitro on thoracic aortae. 3 Maximum contractile response to phenylephrine of endothelium-intact thoracic aortic rings (passive tension 1.0 g) obtained from swimming rats (1.2 ± 0.2 g, n = 8) was lower than that of sedentary control rats (2.1 ± 0.2 g, n = 8). When the endothelium was removed, however, the dose-response curves of both groups of rats were shifted to the left with an increase in maximum responses and they were no longer significantly different (max. tension, swimming rats: 3.2 ± 0.3 g, n = 6, control rats: 3.4 ± 0.4 g, n = 5). 4 Indomethacin did not significantly alter the dose-response curves. A similar effect to that obtained by removal of the endothelium was observed when methylene blue and indomethacin were both added. 5 Passive tension in the range of 2.5-3.0 g, caused a significant increase in active tension developed to phenylephrine (1 uM for endothelium-intact and 0.1 I M for endothelium-denuded) of thoracic aortic rings of both swimming and sedentary control rats compared to their corresponding groups when using passive tension of 1.0-1.5 g. 6 The reduction in responses to phenylephrine of endothelium-intact thoracic aortic rings of swimming rats persisted with the use of a passive tension of 3.0 g. The presence of 300 JiM N0-nitro-L-arginine (L-NOARG) caused a significant leftward shift of the curve with an increase in maximum responses when a passive tension of either 1.0 or 3.0 g was applied to the rings. However, for the rings with a passive tension of 1.0 g, L-NOARG caused a smaller increase in maximal contractile responses to phenylephrine of the rings of sedentary controls than those of swimming rats. 7 There was no difference in the dose-response curves to depolarizing concentrations of KCl (20, 40, 80 and 120 mM) of endothelium-intact thoracic aortic rings from swimming and sedentary control rats. When the endothelium was removed, however, the dose-response curves of both groups of animals were shifted to the left with an increase in maximum responses. Moreover, the responses to KCl of endothelium-denuded thoracic aortic rings of swimming rats were greater than those of sedentary control rats.8 These results suggest that there were changes in vascular responsiveness to phenylephrine and KCl during exercise.

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Section: Discussionsupporting

confidence: 83%

Effect of swimming on vascular reactivity to phenylephrine and KC1 in male rats

Jansakul

1995

British J Pharmacology

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“…Besides, canine coronary smooth muscle has been reported to have a lowered responsiveness to vasoactive relaxants after training. 16 Therefore, the enhanced ACh-induced vasorelaxation response was probably not due to an increased sensitivity of vascular smooth muscle to EDRF.…”

Section: Discussionmentioning

confidence: 94%

“…According to the above studies, we speculated that regular aerobic exercise may enhance endothelium-dependent vasorelaxation. In 1991, Rogers et al 16 found a decrease in responsiveness of canine coronary vascular smooth muscle to vasoactive relaxants after exercise training. However, no reports indicate whether endotheliumdependent vasorelaxation response would be altered by exercise training.…”

mentioning

confidence: 99%

Physical conditioning can modulate endothelium-dependent vasorelaxation in rabbits.

Chen

1993

Arterioscler Thromb

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To investigate whether exercise training can modulate endothelium-dependent vasorelaxation, male New Zealand White rabbits were divided into either control or training groups. The training animals were trained on a treadmill with a running speed of 0.88 km/hr on a 0° grade for 10-60 minutes/day, 5 days/week for 8 weeks. After exercise training, the resting heart rate was lowered (p<0.05). At the end of the experiments, three vessel segments, i.e., the thoracic aortas, the pulmonary arteries, and the common carotid arteries, were isolated and precontracted with norepinephrine. Acetylcholine-stimulated endothelium-derived relaxing factor (EDRF) release was assessed by bioassay in the presence of indomethadn (10~s M). Basal release of EDRF was examined by the addition of hemoglobin. In addition, the relaxing responses of the thoracic aortas and pulmonary arteries to A23187, a calcium ionophore, and to sodium nitroprusside, a direct vasodilator of vascular smooth muscle, were compared between control and trained groups to further investigate possible underlying mechanisms. The results indicated that after exercise training 1) both the thoracic aorta and pulmonary artery, but not the carotid artery, became more sensitive to acetylcholine-induced vasorelaxation; 2) no significant differences in basal release of EDRF between control and trained rabbits were observed; and 3) there were no significant differences in the vascular responses to A23187 or sodium nitroprusside between the two groups. Our data suggest that exercise training may enhance endothelium-dependent vasodilation to acetylcholine via the stimulated EDRF release and that this elevated sensitivity to acetylcholine may not be caused by the alteration of the relaxing response in vascular smooth muscle. (Arteriosclerosis and Thrombosis 1993;13:852-856) KEY WORDS • endurance exercise • endothelium • acetylcholine • rabbits • endotheliumderived relaxing factor

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“…Franke et al (22) found that ExT enhanced eNOS-dependent increases in forearm vascular conductance but did not alter vascular responses to eNOS-dependent agonists. In addition, Oltman et al (47) found that ExT did not influence NOS-dependent responses of porcine coronary arteries, and Rogers et al (53) report that ExT actually decreased responsiveness of isolated canine coronary arteries to ␤-adrenergic agonists. Furthermore, we have reported that ExT does not alter eNOS-dependent dilation of the basilar artery in nondiabetic rats (43).…”

Section: Discussionmentioning

confidence: 99%

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

Mayhan

Arrick

Patel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Mayhan WG, Arrick DM, Patel KP, Sun H. Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats. Am J Physiol Heart Circ Physiol 300: H1013-H1020, 2011. First published December 17, 2010; doi:10.1152/ajpheart.00873.2010.-Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we measured superoxide anion levels in brain tissue under basal conditions in sedentary and exercised nondiabetic and diabetic rats. Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. We found that ADP and NMDA produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic rats. In contrast, ADP and NMDA produced only minimal vasodilation in sedentary diabetic rats. ExT restored impaired ADP-and NMDA-induced vasodilation observed in diabetic rats to that observed in nondiabetics. Nitroglycerin produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic and diabetic rats. Superoxide levels in cortex tissue were similar in sedentary and exercised nondiabetic rats, were increased in sedentary diabetic rats, and were normalized by ExT in diabetic rats. Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. We conclude that ExT can alleviate impaired eNOS-and nNOS-dependent responses of pial arterioles during T1D. adenosine 5=-diphosphate; N-methyl-D-aspartate; nitroglycerin; pial arterioles; Western blot; superoxide; endothelial nitric oxide synthase; neuronal nitric oxide synthase EXERCISE TRAINING (ExT) has been shown to play a significant role in the prevention of cardiovascular-related diseases. Although the precise cellular/molecular mechanisms accounting for the favorable effects of ExT on the cardiovascular system remain uncertain, many investigators have suggested that ExT may dramatically influence vascular endothelial function. Support for this concept can be found in studies that have examined the effects of ExT on endothelial nitric oxide synthase (eNOS)-dependent vasoreactivity in animals and human subjects (22,23,27,28,60,69). These studies have reported that ExT can enhance eNOS-dependent responses of large and small blood vessels in skeletal muscle, heart, and skin. Mechanisms by which ExT potentiates nitric oxide synthase (NOS)-dependent relaxation/dilation of blood vessels are not entirely clear but are likely to be related to an increase in shear forces actin...

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Exercise training and responsiveness of isolated coronary arteries

Cited by 48 publications

References 0 publications

Effect of swimming on vascular reactivity to phenylephrine and KC1 in male rats

Effect of swimming on vascular reactivity to phenylephrine and KC1 in male rats

Physical conditioning can modulate endothelium-dependent vasorelaxation in rabbits.

Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

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