Cardioprotective effect of valsartan in mice with short-term high-salt diet by regulating cardiac aquaporin 1 and angiogenic factor expression

Jiang, Yong; Wang, Huiyan; Zheng, Shouguo; Mu, Shang-qiang; Ma, Mengni; Xie, Xiumin; Zhang, Yangyang; Zhang, Chun-xue; Cai, Jianhui

doi:10.1016/j.carpath.2014.12.003

Cited by 9 publications

(7 citation statements)

References 32 publications

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“…Aquaporin1 is the major water channel in renal proximal tubule and loop of Henle that is responsible for reabsorbing 80% of glomerular filtrate [75, 76]. It has been reported that renal and cardiac AQP1 expressions were downregulated in conditions such as renal fibrosis in mice [77] and HS-induced HPN [78]. The present result is in accordance with the finding by Penna et al [79] who showed that 8% HS downregulated APQ1.…”

Section: Discussionsupporting

confidence: 91%

Effect of high-salt diet on mean arterial pressure, renal epithelial sodium channels and aquaporin subunits expression levels in Spontaneously Hypertensive Rats

Ramachandran

Gholami

Lam

et al. 2019

Preprint

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27An increase in blood pressure (BP) by a high-salt (HS) diet may involve the 28 changes in the expression of epithelium sodium channels (ENaCs) and aquaporins 29 (AQPs) in the kidney which affect the sodium-and water-handling mechanisms. In the 30 present study, spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats 31 were exposed to HS and regular-salt (RS) diets for 6 weeks and fluid intake was 32 monitored. After 6 weeks, mean arterial pressure (MAP) and plasma hormonal activity 33 of atrial natriuretic peptide (ANP), levels of angiotensin II (Ang II), aldosterone and 34 arginine vasopressin (AVP) were determined. The expression of mRNA and protein 35 levels of ENaC and AQP subunits in kidneys were quantified by real-time PCR and 36 Western blotting. High-salt diet caused higher MAP only in SHRs and higher fluid 37 intake in both strains of rats when compared with their respective controls on RS diet.38 The plasma levels of Ang II and aldosterone were low in both SHRs and WKY rats fed 39 with HS diet. Meanwhile, plasma ANP activity was high in both strains of rats on HS 40 diet; whilst the AVP showed vice versa effects. The renal expression of mRNA and 41 protein levels of α-and γ-ENaCs was lowered by HS diet in both SHRs and WKY rats.42 Although β-ENaC mRNA and protein expression levels were depressed in SHRs but 43 they were enhanced in WKY rats. On the other hand, AQP-1, 2 and 7 mRNA and 44 protein expression levels were lowered in both strains of rats fed with HS diet, while 45 that of AQP-3, 4 and 6 showed no significant changes. The suppression of mRNA and 46 protein expression levels of ENaC and AQP subunits suggests that the HS-induced 47 increase in the MAP of SHRs may not be due to the renal sodium and water retention 48 solely. 49 3 50 Introduction 51 Dietary salt (i.e. sodium chloride, NaCl) intake is the most remarkably modifiable 52 environmental risk factor that attracts many studies on hypertension (HPN). It has been 53 acknowledged as an important contributing factor of the aetiology and progression of 54 HPN [1]. Despite the abundant experimental, interventional and epidemiological 55 observations demonstrating an association between dietary salt and HPN, scepticism 56 remains as to how high salt (HS) intake can be mechanistically linked to the increase in 57 blood pressure (BP). Knowing the heterogeneity of HPN, it is likely to involve the 58 intricate integration of multiple regulatory systems and the kidneys have long been 59 implicated to play a central role in regulating BP. Defects in the kidneys sodium-and 60 water-handling mechanisms have been mooted as one of the primary causes of HPN in 61 HS intake [2]. 62The kidneys have the capacity to return altered BP to baseline level by 63 increasing or decreasing sodium and water excretion in response to elevated or reduced 64 BP [3]. This is accomplished in the kidney by the presence of renal membrane-bound 65 protein i.e. epithelial sodium channel (ENaC) that fine-tune sodium reabsorption [4] 66 and aquaporins (AQPs) that ...

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Section: Discussionsupporting

confidence: 91%

Effect of high-salt diet on mean arterial pressure, renal epithelial sodium channels and aquaporin subunits expression levels in Spontaneously Hypertensive Rats

Ramachandran

Gholami

Lam

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…In addition, we found that the body weight, food and water intake, and blood glucose were significantly altered by HS diet. Our observation in combination with previous studies suggest a broad physiological and behavioral influence of HS diet on rodents, although these animals may develop mechanisms to circumvent blood pressure increase by high dietary salt .…”

Section: Discussionsupporting

confidence: 81%

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

Wang

et al. 2017

Molecular Nutrition Food Res

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ScopeA high salt (HS) diet is detrimental to cognitive function, in addition to having a role in cardiovascular disorders. However, the method by which an HS diet impairs cognitive functions such as learning and memory remains open.Methods and resultsIn this study, we found that mice on a 7 week HS diet demonstrated disturbed short‐term memory in an object‐place recognition task, and both 4 week and 7 week HS treatments impaired long‐term memory, as evidenced in a fear conditioning test. Mechanistically, the HS diet inhibited memory‐related long‐term potentiation (LTP) in the hippocampus, while also increasing the levels of reactive oxygen species (ROS) in hippocampal cells and downregulating the expression of synapsin I, synaptophysin, and brain‐derived neurotrophic factor in specific encephalic region.ConclusionThis suggests that oxidative stress or synaptic protein/neurotrophin deregulation was involved in the HS diet‐induced memory impairment. Thus, the present study provides novel insights into the mechanisms of memory impairment caused by excessive dietary salt, and underlined the importance of controlling to salt absorb quantity.

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“… 9 Moreover, in the mouse model of hypertension induced by a high-salt diet, the reduction of cardiac AQP1 might be associated with hypertension and cardiac injury, because angiotensin-receptor blocker treatment (valsartan) partially reversed the effects of a high-salt diet on hypertension with cardiac damage (fibrosis and inflammatory cell infiltration) and normalised cardiac AQP1 expression. 10 …”

Section: Discussionmentioning

confidence: 99%

“… 7 , 8 In contrast, recent studies reported that renal and cardiac AQP1 expression was downregulated and associated with renal fibrosis 9 and high-salt diet-induced hypertension. 10 Thus, it remains unclear whether AQP1 expression can directly or indirectly affect blood pressure and kidney injury.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of angiotensinogen downregulates aquaporin 1 expression via modulation of Nrf2–HO-1 pathway in renal proximal tubular cells of transgenic mice

Chang

Zhao

et al. 2016

J Renin Angiotensin Aldosterone Syst

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Introduction:We aimed to examine the regulation of aquaporin 1 expression in an angiotensinogen transgenic mouse model, focusing on underlying mechanisms.Methods:Male transgenic mice overexpressing rat angiotensinogen in their renal proximal tubular cells (RPTCs) and rat immortalised RPTCs stably transfected with rat angiotensinogen cDNA were used.Results:Angiotensinogen-transgenic mice developed hypertension and nephropathy, changes that were either partially or completely attenuated by treatment with losartan or dual renin–angiotensin system blockade (losartan and perindopril), respectively, while hydralazine prevented hypertension but not nephropathy. Decreased expression of aquaporin 1 and heme oxygenase-1 and increased expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and sodium–hydrogen exchanger 3 were observed in RPTCs of angiotensinogen-transgenic mice and in angiotensinogen-transfected immortalised RPTCs. These parameters were normalised by dual renin–angiotensin system blockade. Both in vivo and in vitro studies identified a novel mechanism in which angiotensinogen overexpression in RPTCs enhances the cytosolic accumulation of Nrf2 via the phosphorylation of pGSK3β Y216. Consequently, lower intranuclear Nrf2 levels are less efficient to trigger heme oxygenase-1 expression as a defence mechanism, which subsequently diminishes aquaporin 1 expression in RPTCs.Conclusions:Angiotensinogen-mediated downregulation of aquaporin 1 and Nrf2 signalling may play an important role in intrarenal renin–angiotensin system-induced hypertension and kidney injury.

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Cardioprotective effect of valsartan in mice with short-term high-salt diet by regulating cardiac aquaporin 1 and angiogenic factor expression

Cited by 9 publications

References 32 publications

Effect of high-salt diet on mean arterial pressure, renal epithelial sodium channels and aquaporin subunits expression levels in Spontaneously Hypertensive Rats

Effect of high-salt diet on mean arterial pressure, renal epithelial sodium channels and aquaporin subunits expression levels in Spontaneously Hypertensive Rats

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

Overexpression of angiotensinogen downregulates aquaporin 1 expression via modulation of Nrf2–HO-1 pathway in renal proximal tubular cells of transgenic mice

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