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

Abstract

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 ...

Effect of Angiotensin receptor blockade on Plasma Osmolality and Neurohumoral Responses to High Environmental Temperature in Rats Fed a High Salt Diet

“…Meanwhile, our current result showed that plasma angiotensin II and aldosterone levels were raised in the rats fed with high salt diet, similar to the inappropriate activation of these hormones reported by Gonsalez et al (2018). But this was in disagreement with the suppressed levels of these hormones reported by Stocker et al, (2003) and Ramachandran et al (2019).…”

“…Generally, blockers of AT1 receptor possess antiadrenergic potential to attenuate catecholamine level (Diz et al, 201;Balt et al, 2002). In support of this, earlier investigation revealed that AT1 receptor antagonist blunted Central Nervous SympatHETic activity in experimental animals with heart disease (Ramachandran et al, 2019). Averill et al (1994) also demonstrated that losartan, an AT1 receptor antagonist, attenuated pressor and sympatHETic overactivity induced by angiontensin II in spontaneous hypertensive rats.…”