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Objective:To explore the effect of regular aerobic exercise on renal fibrosis and its mechanism.Methods:Thirty male Sprague-Dawley rats were randomly divided into a young control group (YC group), an old control group (OC) and an old exercise group (OE), each of 10. The YC and OC groups were kept quietly in cages, while the OE group performed moderate-intensity treadmill aerobic exercise for 8 weeks. After the experiment, renal function was evaluated by measuring 24h urine protein, blood urea nitrogen (BUN) and serum creatinine (SCr). The degree of renal fibrosis was detected by Masson staining, and the expressions of transforming growth factor β 1 (TGF- β 1), p38 mitogen-activated protein kinase (p38MAPK), phosphorylated p38MAPK (p-p38MAPK), E-cadherin, and α-smooth muscle actin (α-SMA) were measured using western blotting. Results:Compared with the YC group, a significant increase was observed in the OC group in average 24h urine protein, BUN and SCr, but also in the degree of renal fibrosis, the protein expression of TGF-β 1, p-p38MAPK and α-SMA. There was a significant decrease in the average expression of E-cadherin. Compared with the OC group, the average 24h urine protein, BUN and SCr, the degree of renal fibrosis, the expression of TGF-β 1, p-p38MAPK and α-SMA protein had all decreased significantly in OE group, while the average expression of E-cadherin had increased significantly. Conclusions:Aerobic exercise relieves renal fibrosis in elderly rats, perhaps through inhibiting the TGF-β 1/p38MAPK signaling pathway and epithelial-mesenchymal transition.
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Objective@#To observe the effect of high-intensity interval training (HIIT) on G protein-coupled receptor kinase-2 (GRK2) levels in the hearts and adrenal glands of spontaneously hypertensive rats (SHRs) and explore how exercise might improve sympathetic over-excitation.@*Methods@#Twenty male SHRs were divided randomly into a sedentary control group and an HIIT group. Ten age-matched, male Wistar-Kyoto rats without hypertension served as the control group. The rats of the control and sedentary control groups were housed in cages at rest while those of the HIIT group underwent eight weeks of HIIT. Caudal artery pressure, cardiac structure and function, and heart rate variability (HRV) were determined using a non-invasive blood pressure tester, echocardiograms, and electrocardiograms. The plasma concentrations of epinephrine and norepinephrine, and the expression of GRK2 and β1-adrenoceptor (β1-AR) protein were measured in the rats′ hearts, and GRK2 and α2-adrenoceptor (α2-AR) protein were measured in their adrenal glands using high-pressure liquid chromatography and western blotting.@*Results@#Compared with the normotensive control group, animals in the sedentary control group showed elevated blood pressure, cardiac hypertrophy, reduced heart function, sympathetic over-excitation manifested by HRV, increased plasma epinephrine and norepinephrine concentrations, up-regulated GRK2 protein expression in the heart and adrenal gland, but down-regulated β1-AR in the heart and down-regulated α2-AR in the adrenal gland. Compared with the sedentary control group, the HIIT group did not show improved cardiac hypertrophy, but it did show reduced blood pressure, enhanced heart function, suppressed sympathetic over-excitation, as well as lowered plasma epinephrine and norepinephrine concentrations, on average. The expression of GRK2 in the heart and adrenal gland was significantly down-regulated, while that of β1-AR in the heart and of α2-AR in the adrenal gland were significantly up-regulated, on average.@*Conclusions@#HIIT can alleviate sympathetic over-excitation and enhance heart function despite spontaneous hypertension, at least in rats. The therapeutic mechanism may be related with the down-regulation of GRK2 expression in the heart and adrenal gland.
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Objective To explore the effect of exercise on functional sympatholysis in rats modeling spontaneous hypertension and the role of the nitric oxide signal pathway. Methods Thirty Wistar rats with spontaneous hypertension were randomly divided into a sedentary group and an exercise group, each of 15, while another fifteen healthy rats acted as controls. The exercise group performed eight weeks of voluntary wheel run-ning exercise while the other two groups did not. The rats were instrumented to stimulate the lumbar sympathetic chain ( at 1 Hz, 2.5 Hz or 5 Hz) to induce vasoconstriction and the triceps surae muscle group was forced to contract by stimulating the tibial nerve electrically. The change in the femoral artery vascular conductance ( FAVC) in response to sympathetic stimulation was recorded at rest and during contraction. The functional sym-patholysis was calculated as the percentage difference in FAVC (△％FAVC) in response to sympathetic stimu-lation during muscular contraction and at rest (△％FAVC=％FAVC during contraction-％FAVC at rest) . After administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester ( L-NAME) , changes in FAVC were repeatedly determined. Results The average △％FAVC of the sedentary group was significantly lower than that of the control group at all stimulation frequencies, while the average △％FAVC in the exercise group was significantly higher than in the sedentary group. There were no significant differences between the exer-cise and control groups. After the administration of L-NAME, significant decrease was observed in the average△％FAVCs of the control and exercise groups, but there was no significant change in the sedentary group. Conclusion Voluntary exercise may improve functional sympatholysis in rats with spontaneous hypertension through improving NO-dependent signalling.