Time-Course of Neuroendocrine Changes and Its Correlation with Hypertension Induced by Ethanol Consumption

Abstract

Taken together, these results suggest that increased sympathetic activity may contribute to the early increase in MAP observed in ETOH-treated rats. However, the maintenance of this effect may be predominantly regulated by the long-term increase in the secretion of other circulating factors, such as AVP and ANG II, the secretion of both hormones being stimulated by the ETOH-induced dehydration.

Heavy Alcohol Consumption Effects on Blood Pressure and on Kidney Structure Persist After Long-Term Withdrawal

“…Heavy ethanol consumption effects on BP were predictable on the basis of data from our [14] and others studies [8, 12]. In the present study, we extend those observations by showing that the hypertensive effect of ethanol consumption was not completely reversed after long-term ethanol withdrawal.…”

“…Chronic ethanol consumption elevates BP through different mechanisms [5, 8, 11, 12], including the activation of the renin-angiotensin system (RAS) [11, 21, 22], oxidative stress [11, 12, 18, 21-23] and enhancement of the sympathetic nerve activity [5]. Most of the angiotensin II (Ang II) evoked effects are mediated by Ang II type 1 receptor (AT1R) [21, 22, 24, 25], such as elevation of systemic BP, vasoconstriction, inhibition of renal sympathetic nerve activity, baroreceptor control, glomerular hypertension, and retention of sodium and body fluids [22, 24-26].…”

nNOS is involved in cardiac remodeling induced by chronic ethanol consumption

“…Indeed, the asymptomatic alcoholic cardiomyopathy is clinically expressed by impaired left ventricle function (Kloner and Rezkalla, 2007;Laonigro et al, 2009;Piano and Phillips, 2014). Regarding the repercussions of alcohol consumption on body weight and on food intake, there was a progressive increase in body weight and in the amount of food intake in ethanol-treated rats, as it was observed by others (Da Silva et al, 2013;Silva et al, 2009). Even so, at the end of the experimental period, ethanol-treated rats were lighter than the respective controls.…”

“…** P < 1 Â10 À4 . direct measurements (Da Silva et al, 2013;Resstel et al, 2006), even after short periods of ethanol treatment (Da Silva et al, 2013;Husain et al, 2008;Resstel et al, 2006). It is well documented that the increase of RAS activity and of sympathetic nerve activity underlies both hypertension and cardiac remodeling (Hering et al, 2011;Malpas, 2010).…”

“…Studies in humans and in animal models have shown increased myocyte loss (due to apoptosis), intracellular organelle dysfunction, impaired protein synthesis and activity, and impaired calcium homeostasis in hearts exposed to high concentrations of ethanol (Fernández-Solà et al, 2006;Fogle et al, 2010;Jing et al, 2012;Laonigro et al, 2009;Piano and Phillips, 2014;Tan et al, 2012;Vary et al, 2007). Other effects of chronic ethanol consumption include activation of the sympathetic nervous system and renin-angiotensin system (RAS) (Da Silva et al, 2013;Husain et al, 2008;Resstel et al, 2006;Tan et al, 2012), and variable changes in cardiac natriuretic peptide levels (Da Silva et al, 2013;Guillaume et al, 1996;Kim et al, 2001Kim et al, , 2003. There is evidence that ethanol consumption enhances sympathetic activity (Resstel et al, 2006), which leads to cardiac dysfunction and remodeling (Li and Ren, 2008) and, consequently, to further deterioration of heart disease (Malpas, 2010).…”