Objective: Exercise training has antihypertensive and renoprotective effects in humans and rats. However, the effects of exercise training on renal disorders that occur with salt-sensitive hypertension remains unclear. The study aim was to investigate the effects and mechanisms of exercise training on renal function in a rat model of salt-sensitive hypertension. Methods: Six-week-old male Dahl salt-sensitive rats were divided into normal-salt (0.6% NaCl) diet, high-salt (8% NaCl) diet, and high-salt diet with exercise training groups. The high-salt diet with exercise training group underwent daily treadmill running for 8 weeks. Results: The high-salt diet induced severe hypertension and renal dysfunction. Exercise training significantly improved high-salt diet-induced urinary protein, albumin, and l-type fatty acid-binding protein excretion, and glomerulosclerosis but not renal interstitial fibrosis without changing blood pressure. Exercise training significantly attenuated high-salt diet-induced oxidative stress in the kidneys and decreased high-salt diet-stimulated xanthine oxidoreductase activity but not nicotinamide adenine dinucleotide phosphate oxidase activity. The high-salt diet did not change urinary excretion of 20-hydroxyeicosatetraenoic acid and decreased cytochrome P450 4A protein expression in the kidneys. Exercise training increased urinary 20-hydoroxyeicosatetraenoic acid excretion and renal cytochrome P450 4A protein expression. Conclusion: Exercise training improved renal disorders without lowering blood pressure in Dahl salt-sensitive rats. Exercise training also decreased oxidative stress and increased 20-hydroxyeicosatetraenoic acid production in the kidneys. These results suggest that improvements in oxidative stress and 20-hydroxyeicosatetraenoic acid production may be potential mechanisms by which exercise training improved renal disorders in Dahl salt-sensitive rats.
An association between respiratory muscle weakness and sarcopenia may provide a clue to the mechanism of sarcopenia development. We aimed to clarify this relationship among community-dwelling older adults. In total, 117 community-dwelling older adults were assessed and classified into 4 groups: robust, respiratory muscle weakness, sarcopenia, and respiratory sarcopenia. The respiratory sarcopenia group (12%) had a significantly higher percentage of males and had lower BMI, skeletal muscle index, skeletal muscle mass, phase angle, and oral function than the robust group (32.5%). All physical functions were significantly lower. The respiratory muscle weakness group (54.7%) had a significantly lower BMI and slower walking speed, compared with the robust group. The sarcopenia group (0.8%) was excluded from the analysis. The percent maximum inspiratory pressure was significantly lower in both the respiratory muscle weakness and respiratory sarcopenia groups, compared with the robust group. Almost all participants with sarcopenia showed respiratory muscle weakness. In addition, approximately 50% had respiratory muscle weakness, even in the absence of systemic sarcopenia, suggesting that respiratory muscle weakness may be the precursor of sarcopenia. The values indicating physical function and skeletal muscle mass in the respiratory muscle weakness group were between those in the robust and the respiratory sarcopenia groups.
BACKGROUND Xanthine oxidase (XO) is a source of reactive oxygen species production in the heart. However, pathophysiological role of XO has not been clarified in hypertensive heart disease. Thus, the present study examined the impacts of high salt (HS) intake and febuxostat (Fx), a XO inhibitor in Dahl salt-sensitive (Dahl-S) rats. METHODS Eight-week old, male Dahl-S rats were fed a normal salt diet (0.6% NaCl) or a HS diet (8% NaCl) for 8 weeks. A part of the rats fed the HS diet were simultaneously treated with Fx (3 mg/kg/day). RESULTS HS intake increased blood pressure and heart weight with cardiomyocyte hypertrophy and interstitial fibrosis in the left ventricle (LV), and Fx diminished them. HS increased the XO activity 4.7-fold and nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity 1.5-fold, and Fx not only blocked the XO activity but also inhibited the HS-increased NADPH oxidase activity. HS increased the expression of XO, collagen, transforming growth factor-β1 (TGF-β1), angiotensin-converting enzyme, and angiotensin II type 1 receptor and the phosphorylation of extracellular signal-regulated kinase (ERK) in the LV, and Fx reduced the expression and phosphorylation of these proteins except XO. CONCLUSIONS Fx ameliorates the HS intake-induced hypertension, LV hypertrophy, and fibrosis with decreasing the TGF-β1 expression and ERK phosphorylation in Dahl-S rats. Fx also down-regulates cardiac NADPH oxidase and renin–angiotensin system. The XO inhibition may be an effective therapy for hypertensive heart disease.
Purpose: Exercise training (Ex) has antihypertensive and renal protective effects; however, the precise mechanisms remain unclear. The renal renin-angiotensin system (RAS) plays a vital role in renal function and pathology. Therefore, we investigated the effects of Ex on the renal RAS components in Dahl salt-sensitive (Dahl-S) rats. Methods: Male Dahl-S rats were divided into four groups: normal salt diet + sedentary, normal salt diet + Ex, high-salt diet (HS, 8% NaCl) + sedentary, and HS + Ex. Treadmill running was performed for 8 wk in the Ex groups. Results: Ex attenuated the HS-induced renal dysfunction and glomerular injury without causing blood pressure alterations. HS increased urinary excretion of both total and intact angiotensinogen. Ex decreased the HS-induced increased urinary excretion of total angiotensinogen. However, it did not change the HS-induced urinary excretion of intact angiotensinogen, indicating reduced intact angiotensinogen cleaving. Ex restored the HS-induced increased angiotensinogen and angiotensin II type 1 receptor expressions in the outer medulla and the HS-induced increased angiotensin-converting enzyme expression in the cortex. Ex restored the HS-induced decreased renin expression in the cortex and outer medulla, and the HS-induced decreased angiotensin-converting enzyme 2, angiotensin II type 2 receptor, and Mas receptor expressions in the outer medulla. Conclusions: Ex attenuates HS-induced renal dysfunction, glomerular injury, and renal RAS dysregulation in Dahl-S rats.
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