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

Abstract

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.

Vascular Sensitivity to Phenylephrine in Rats Submitted to Anaerobic Training and Nandrolone Treatment

“…Abdominal aorta obtained from treadmilltrained rabbits presented higher endothelium-dependent vasorelaxation induced by acetylcholine (ACh). Thoracic aorta from rats submitted to swimming during 6 weeks showed a decrease in response to PE, but not to potassium chloride, 25 as also reported in porcine coronary arteries. 26 The aortic subsensitivity to PE observed after anaerobic training in the present study suggests that even in response to the metabolic demands of different physical exercises (aerobic versus anaerobic), vascular adaptations are established to promote a decrease in arterial blood pressure.…”

“…20,23 Thoracic aortas isolated from swimming trained rats were also subsensitive to PE, and this effect was caused by an increase in NO production by endothelial cells. 25 Delp and Laughin 21 reported an upregulation of the expression of endothelial cell NOS mRNA in thoracic aorta from rats submitted to 4 to 10 weeks of training. These results are consistent with others who have reported an increase in NOS mRNA levels in aorta of exercise-trained dogs, 28 and in coronary resistance vessels of exercise-trained pigs.…”

Vascular adaptive responses to physical exercise and to stress are affected differently by nandrolone administration

“…In fact, the acute exposure to stress reduced the aortic reactivity to noradrenaline of sedentary rats that was abolished by endothelium removal. These findings support published reports showing a decreased reactivity to vasopressor agents dependent on the integrity of endothelial cells under stress conditions, and confirm earlier findings from our laboratory (15,19,36). Although stress and physical exercise alone induced aortic hyporeactivity to noradrenaline, the association of the two conditions did not result in a synergistic effect.…”

Exhaustive swimming differentially inhibits P2X1 receptor- and α1-adrenoceptor-mediated vasoconstriction in isolated rat arteries

“…It has been reported that long-term swimming exercise significantly reduces the vasoconstrictive response to phenylephrine in the rat mesenteric artery and thoracic aorta when the endothelium is intact, but not in the endothelium-denuded arteries [26,27] . Chronic exercise also enhances endotheliummediated vasodilatation in the endothelium-intact aorta and mesenteric artery, but this exercise does not affect NA-induced vasoconstriction in the endothelium-denuded arteries isolated from spontaneously hypertensive rats [28] .…”