Long-term exercise attenuates blood pressure responsiveness and modulates kidney angiotensin II signalling and urinary sodium excretion in SHR

Abstract

Observations have been made regarding the effects of long-term exercise training on blood pressure, renal sodium handling and renal renin-angiotensin-aldosterone (RAS) intracellular pathways in conscious, trained Okamoto-Aoki spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKy) normotensive rats, compared with appropriate agematched sedentary SHR and WKy. To evaluate the influence of exercise training on renal function and RAS, receptors and intracellular angiotensin II (AngII) pathway compounds were used respectively, and lithium clearance and western blot methods were utilised. The current study demonstrated that increased blood pressure in SHR was blunted and significantly reduced by long-term swim training between the ages of 6 and 16 weeks. Additionally, the investigators observed an increased fractional urinary sodium excretion in trained SHR (SHR T ) rats, compared with sedentary SHR (SHR S ), despite a significantly decreased creatinine clearance (C Cr ). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1 R in the entire kidney of T SHR rats, compared with S SHR . Conversely, the expression of the AT2 R , in both sedentary and trained SHR, was unchanged. The present study may indicate that, in the kidney, long-term exercise exerts a modulating effect on AngII receptor expression. In fact, the present study indicates an association of increasing natriuresis, reciprocal changes in renal AngII receptors and intracellular pathway proteins with the fall in blood pressure levels observed in T SHR rats compared with age-matched S SHR rats.

Chronic exercise modulates RAS components and improves balance between pro- and anti-inflammatory cytokines in the brain of SHR

“…Because role of AngII is well established in regulation of renal excretion of water and electrolyte, exercise-induced increase in urinary sodium excretion could also attribute to pressure-lowering effects of exercise. For instance, Ciampone et al (2011) have recently reported an association between reduced BP, increased natriuresis, and improvement in renal RAS components[8]. It is also important to discuss that adipocytes are known to play an important role in cytokine production and a recent study reported increased ACE expression by adipocyte-derived lipid mediators in macrophages [32].…”

Renal sodium handling and blood pressure changes in gestational protein-restricted offspring: Role of renal nerves and ganglia neurokinin expression

“…Inc, MA, USA), respectively. Thereafter, animals were anaesthetized with ketamine and xylazine injected intraperitoneally and sacrificed by cardiac puncture; urine and plasma samples were stored for analysis [3,4,6,7,29,30]. …”

“…Fractional sodium excretion (FE Na ) was calculated as C Na /C Cr ×100, where C Na is sodium clearance. Fractional proximal (FEP Na ) and post-proximal (FEPP Na ) sodium excretion were calculated as C Li /C Cr × 100 and C Na /C Li × 100, respectively [3,4,6,7,29,30]. Data obtained over time were analyzed using two-way ANOVA or nonparametric analysis using the Kruskal–Wallis test.…”

Tissue Renin–Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease

“…Studies in rodents find chronic exercise to inhibit tissue RAS activation in the brain (58) (reduced local ACE and AT 1 R), heart (59, 60) (reduced local ACE and ANG II), and kidney (reduced local AT 1 R) (61). These findings suggest that down-regulation of tissue RAS may partly mediate the beneficial effects related to frequent exercise.…”