Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model

Abstract

The study aim was to investigate the interaction of physical conditioning and chronic ethanol ingestion on blood pressure (BP), heart rate (HR), nitric oxide (NO) and oxidants/antioxidants balance in the plasma of rats. Male Fisher rats were divided into four groups of seven animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks; (2) ethanol (4 g kg(-1), orally) daily for 12 weeks; (3) exercise training on treadmill plus sucrose daily for 12 weeks and (4) exercise training on treadmill followed by ethanol (4 g kg(-1), orally) daily for 12 weeks. The body weight, BP and HR were recorded every week. The animals were sacrificed under ether anesthesia after 12 weeks, blood collected in heparinzed vials, plasma isolated and analyzed. The results show that exercise training significantly lowered the weight gain 6-12 weeks in ethanol treated rats compared to ethanol alone or control rats. The mean arterial BP was significantly elevated 6-12 weeks after ethanol ingestion without significant alterations in HR. Exercise training lowered the BP close to the normal control values in ethanol fed rats. Ethanol significantly decreased the plasma NO levels, reduced to oxidized glutathione ratio (GSH/GSSG) and antioxidant enzymes-superoxide dismutase (CuZn-SOD, and Mn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities while plasma NADPH oxidase activity and malondialdehyde (MDA) levels were significantly elevated compared to control. Exercise training significantly restored the depletion of plasma NO levels, GSH/GSSG ratio, and antioxidant enzyme activities and normalized the MDA levels and NADPH oxidase activity in the plasma of ethanol treated rats. The study concluded that physical conditioning attenuates the chronic ethanol-induced hypertension by augmenting the NO bioavailability and reducing the oxidative stress response in the plasma of rats.

Alcohol-induced hypertension: Mechanism and prevention

“…The magnitude of the increase in blood pressure in heavy drinkers averages about 5 to 10 mmHg, with systolic increases nearly always greater than diastolic increases [18] . Similar changes in blood pressure were also reported in preclinical studies [19][20][21][22] . In the Framingham cohort [23,24] , there was an increase of 7 mmHg in mean arterial pressure when heavy alcohol users were compared with all others.…”

“…In the endothelium, depletion of NO production or NO reaction with superoxide anion to form toxic peroxynitrite radical which causes endothelial injury, impairment and hypertension in alcohol treated rats [20][21][22]62,80,94] . Recent studies have shown that chronic ethanol ingestion induces hypertension which was related to increased aortic inflammation, elevated angiotensin II levels, induction of NADPH oxidase causing endothelial injury, depletion of antioxidants, down-regulation of endothelial NO generating system and impaired vascular relaxation in rats [6,[19][20][21][22]62,80] . This mechanism is most likely implicated in chronic alcohol-induced hypertension.…”

“…Exercise increases the utilization of oxygen in the body and up-regulate the antioxidant defense system in the cardiovascular system [97][98][99][100] . Exercise training also generates NO in the cardiovascular system by induction of nitric oxide synthase [19,79,90,101] . Recent studies have shown the beneficial role of physical training in the control of blood pressure in humans [97,98,102,103] and experimental animals [79,90,104,105] .…”

“…Physical inactivity and overweight trigger hypertension [106,107] whereas; regular physical activity has been shown to decrease the BP and body weight [102,103] . Stud- ies have shown that physical conditioning is beneficial in lowering the BP through suppression of weight gain in chronic ethanol treated hypertensive rats [19,79] . Physical conditioning attenuates the chronic ethanol-induced hypertension by augmenting the NO bioavailability and reducing the oxidative stress response in rats [19,79,108] .…”

Adverse Effects of Chronic Alcohol Consumption

“…As a result, the superoxide ions were significantly high due to antioxidant enzyme inhibition. The superoxide ions are able to interact with NO (nitric oxide) to form peroxynitrate which has a wider range of free radical potentials [13]. So, in summary, ethanol performs as an oxidative stress inducer which is the principal cause of hypertension.…”