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

Abstract

Exercise training has reversible beneficial effects on cardiovascular diseases, e.g. hypertension, which may result from a decrease in systemic vascular resistance. The purpose of this study was to investigate possible mechanisms associated with the changes in vascular reactivity in large and small arteries with vasoconstrictors and vasodilators in rats after exercise. Wistar-Kyoto rats were trained for 8 weeks (Ex group) on a treadmill and compared with sedentary counterparts (Sed group). After the measurement of blood pressure and heart rate at 8 weeks, rat mesenteric arteries and thoracic aortas were excised and prepared as rings for this study. In addition, special care was taken not to damage the endothelium of the preparations. Our results showed that exercise training for 8 weeks (1) not only prevented an increase in blood pressure but also caused a fall in heart rate, (2) attenuated the contractions induced by both prostaglandin F_2α (PGF_2α) and high K⁺ in the mesenteric artery, but reduced the PGF_2α-induced contraction in the aorta only, (3) enhanced the relaxation elicited by acetylcholine (ACh) in both mesenteric arteries and aortas, and (4) increased nitrate [an indicator of nitric oxide (NO) formation] in plasma. The enhancement of ACh-induced relaxation in the mesenteric arteries in the Ex group was suppressed by pretreatment with N^ω -nitro-L-arginine methyl ester (L-NAME), tetraethylammonium (TEA; a nonselective inhibitor of K⁺ channels) or charybdotoxin [CTX; a selective inhibitor of large-conductance calcium-activated K⁺ (BK_Ca) channels], whereas in the aorta that response was attenuated by TEA or CTX and almost completely abolished by L-NAME. However, with a combination of L-NAME plus CTX in the mesenteric artery, ACh-induced relaxation was completely abolished in the Sed group, but not in the Ex group. These results suggest that in addition to NO, activation of BK_Ca channels in the vascular beds, at least in part, also contributes to vasodilatation in animals with exercise training.

Erythropoietic responses to a series of repeated maximal dynamic and static apnoeas in elite and non-breath-hold divers

“…In rabbits, endurance exercise reduced renal sympathetic nerve activity, partly, due to enhanced cardiac baroreflex inhibition of sympathetic outflow to the mesenteric and renal circulation (DiCarlo et al 1997; Mueller et al 1998; De Moraes et al 2004). Moreover, in vitro studies examining the conduit arteries and microcirculation of the renal vasculature revealed enhanced production of and/or sensitivity to endogenous endothelial dilators (Chen et al 1999, 2001; Chies et al 2004; De Moraes et al 2004; Moyna and Thompson 2004). Collectively, the insignificant erythropoietic responses in our EBHD group following the static apnoea protocol might be explained by the training-induced renal adaptations and attenuation of renal vasoconstriction.…”