Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Abstract

is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro-and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n ϭ 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n ϭ 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 Ϯ 8% (n ϭ 6; P Ͻ 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 Ϯ 6% (n ϭ 6; P Ͻ 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 Ϯ 8 and 13 Ϯ 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͼ 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with N -nitro-L-arginine methyl ester (L-NAME; 300 M), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 Ϯ 6 and 38 Ϯ 5% for ExT and L-NAME ϩ ExT, respectively (n ϭ 6; P Ͻ 0.05)]. On the other hand, L-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 Ϯ 7 and 45 Ϯ 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͻ 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO. chronic exercise; endothelial dysfunction; isolated perfused rabbit kidney IT IS WELL KNOWN THAT THE endothelium plays a role of paramount importance in the regulation of the vasomotor tone (for review, see Ref. 26). The endothelial cells synthesize and release several relaxing and contracting diffusible substances that interact with the underlying vascular smooth muscle, thus contributing to the continuous modulation of vascular reactivity (26). The best-characterized endothelium-derived relaxing factors are nitric oxide (NO) and prostacyclin (PGI 2 ), which can be released by physical (shear stress by the fl...

Protective Effect of Aerobic Exercise Against L-Name-Induced Kidney Damage in Rats

“…Asghar et al (18) reported that TBARS depletion caused an increase in antioxidant defences and alleviated infl ammation in renal proximal tubules of trained rats. Although the exact mechanisms by which exercise counteracts L-NAME-induced renal injuries are unclear, they may involve increased NO bioavailability and enhanced responsiveness of the renal vascular smooth muscle to NO (28). In fact, under aerobic conditions, NO can inhibit TBARS formation by decomposing primary lipid peroxidation products (29).…”

“…De Moraes et al (28) proposed that increases in cardiac output during exercise, associated with renal vasoconstriction and upregulation of endothelial NOS, could enhance blood fl ow velocity and shear stress in kidney circulation. In addition, they have shown that renal hyperaemia occurring immediately after exercise inactivates vascular ROS and consequently prevents ROS interaction with NO by upregulating free-radical scavenger systems.…”

“…NO bioavailability increased by exercise could be the result of increased activity/expression of eNOS and/or the diminished degradation of NO due to reduced interaction with ROS (33). This phenomenon could be attributed to an elevation of shear stress-induced vasodilation during exercise accompanied by increased blood fl ow (20,28,33).…”

Postnatal exposure to voluntary exercise but not the antioxidant catechin protects the vasculature after a switch to an atherogenic environment in middle-age mice

“…Aging alters both the endothelium and the VSMC [34], and endothelium-independent response can be altered in presence of hyperinsulinemia in patients with metabolic syndrome [64] or by acute hyperhomocysteinemia in diabetic patients [12]. On the other hand, EX has been shown to increase the relaxant response to NO donors in humans and rabbits [15,33], demonstrating that it can reverse and/or counteract the dysfunctional VSMC relaxant capacities. The mechanism involved in the impaired SNP response remains elusive; nonetheless, the equally reduced endothelium-dependent relaxation to Ach was prevented in the presence of indomethacin.…”

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

“…Endurance training of healthy sedentary human subjects results in increased cardiac output and stroke volume (1). Chronic exercise is also known to improve the vasodilatory mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscles, as well as kidney, cutaneous and other vascular beds (2)(3)(4). Decreased blood pressure induced by exercise training was also reported in hypertensive subjects and spontaneously hypertensive rats (5,6).…”