Why the study?
Exercise training has antihypertensive and renal protective effects, but the precise mechanisms and its effects on renal renin-angiotensin system components in salt-sensitive hypertension remain unclear.
Does exercise training improve renal dysfunction and renal renin-angiotensin system dysregulation in Dahl salt-sensitive rats?
Does exercise training improve renal dysfunction and renal renin-angiotensin system dysregulation in Dahl salt-sensitive rats?
Exercise training provides renal protection in salt-sensitive hypertension models by modulating the renal renin-angiotensin system.
Answers are grounded in this paper and cite their sources.
Supports exercise for renal protection in salt-sensitive models; leaves open human translation and RAS-targeted trials.
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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A 2022 study studied this question.
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