Effects of exercise training on responsiveness of the mesenteric arterial bed to phenylephrine and KCl in male rats

Abstract

1 We aimed to determine whether there are any changes in responsiveness of the mesenteric arterial beds to phenylephrine (Phe) and KCl in exercise-trained rats, and whether vascular endothelium and/or vascular smooth muscle play a role in these changes. 2 Adult male rats were subjected to a swimming schedule every day for 28 ± 33 days. Studies were performed in vitro using Krebs perfused mesenteric arterial beds. 3 Maximum perfusion pressure responses to KCl and Phe of the mesenteric arterial beds from exercise-trained rats were signi®cantly lower than those from sedentary controls. However, these di erences disappeared after blocking the nitric oxide synthase by N G -nitro-L-arginine (L-NOARG). 4 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate (CHAPS, 3 mg ml 71 , 2 min infusion) caused a signi®cant increase in maximum perfusion pressure responses to KCl to the same extent in both exercise-trained and sedentary control rats. CHAPS caused about a 4.5 fold leftward shift of the curve with no change in maximum response to Phe for the mesenteric arterial beds from sedentary control rats, but not for those obtained from exercise-trained rats. However, these di erences were abolished in the presence of L-NOARG. 5 Indomethacin did not alter the dose-response curves to KCl or Phe in either swimming or control groups. 6 These results suggest that there was a lower vascular responsiveness to KCl and Phe in exercisetrained rats at rest. The decrease in reactivities to KCl or decrease in sensitivity to Phe after having endothelium impairment by CHAPS of the mesenteric arterial beds of exercise-trained rats were due to an increase in both spontaneous release and upregulation of phenylephrine-stimulated release of nitric oxide from both the vascular endothelium and the vascular smooth muscle cells, and may not be a consequence of an increase in vasodilator prostaglandins by the vascular bed.

Aerobic exercise training increases neuronal nitric oxide release and bioavailability and decreases noradrenaline release in mesenteric artery from spontaneously hypertensive rats

“…To determine this we first analyzed noradrenaline release, observing a huge drop in both basal and EFS-induced noradrenaline release in segments from trained SHRs, in agreement with previous reports describing decreases in plasmatic noradrenaline [38]. Regarding the effect of exercise, increase, decrease and no changes in vasoconstrictor response to alpha-adrenergic agonists have been reported [29][30][31]. In our experimental conditions, we observed that aerobic exercise training increased the vasoconstrictor response to noradrenaline, possibly due to an upregulation process consequent to the decrease in noradrenaline release.…”

“…KCl vasoconstriction is an indicator of the integrity of intrinsic contractile machinery. Previous reports have shown a lower KCl vasoconstriction in resistance arteries isolated from exercise trained rats [29,30], whereas others have found no differences [31]. This discrepancy could be attributed to differences in the vascular bed analyzed and/or kind of training.…”

Exercise Training Activates Large-Conductance Calcium-Activated K^+ Channels and Enhances Nitric Oxide Production in Rat Mesenteric Artery and Thoracic Aorta

“…This enhanced relaxation with ACh after exercise training appears to be mediated by both EDHF and NO. Thus, these mediators may counteract the contraction induced by PGF 2· and high K + in isolated vessels, in particular in small arteries, which is similar to the findings reported by Jansakul and Hirunpan [15]. However, modifications of the participation of prostanoids in this enhanced vasodilatory response were not investigated since the experiments were conducted in the continuous presence of indomethacin.…”

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] .…”

“…Moreover, exercise training increases acetylcholine-induced relaxation and eNOS protein levels in the porcine pulmonary artery [29,30] , but not in the pulmonary artery from hypertensive rats [31] . Therefore, we removed the vascular endothelium of the isolated mesenteric, pulmonary, caudal and internal carotid arteries from the rat to directly observe the changes in α 1 -adrenoceptor-and P2X 1 receptor-mediated vascular smooth muscle contractions because several studies suggest that exercise affects not only the vasoconstriction of vascular smooth muscles [32,33] , but also the function of the vascular endothelium [26,27] . NA induces vasoconstriction and vasodilatation via α-adrenoceptors and β-adrenoceptors.…”