Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Moderate ethanol consumption is known to reduce the risk of cardiovascular diseases; however, chronic high dose ethanol ingestion causes cardiovascular injuries including hypertension. The dose response of ethanol-induced hypertension and associated oxidative stress response has not been well established. This study investigated the dose response of ethanol on blood pressure (BP), nitric oxide (NO) and antioxidants in the plasma of the rat. Male Fisher rats (200-250 g) were divided into five groups of six animals each and treated as follows: (1) control (5% sucrose, orally) daily for 12 weeks; (2) 20-30% ethanol (1 g kg-1, orally) daily for 12 weeks; (3) 20-30% ethanol (2 g kg-1, orally) daily for 12 weeks; (4) 20-30% ethanol (4 g kg-1, orally) daily for 12 weeks; (5) 20-30% ethanol (6 g kg-1, orally) daily for 12 weeks. The BP (systolic, diastolic and mean) was recorded every week through tail-cuff method. The animals were sacrificed 12 weeks after treatments and blood was collected and analyzed. Systolic and mean BP were slightly decreased with 1 g kg-1 dose but significantly elevated with 2, 4 and 6 g kg-1 doses 7-12 weeks after ethanol ingestion. Whereas diastolic BP was significantly elevated with 4 and 6 g kg-1 doses 8-12 weeks after ethanol ingestion. Blood alcohol levels were significantly elevated with 4 and 6 g kg-1 dose of ethanol for 12 weeks. Ethanol dose-dependency increased plasma malondialdehyde (MDA) and protein carbonyl levels, while nitric oxide (NO), ratio of reduced to oxidized glutathione (GSH/GSSG) and antioxidant enzymes: copper/zinc-superoxide dismutase (CuZn-SOD) and manganese (Mn)-SOD, catalase (CAT) and glutathione peroxidase (GSH-Px) activities were decreased 12 weeks post-treatment. The data suggested that ethanol induces hypertension at higher doses by depleting NO and antioxidants and increasing oxidative tissue injury in rats.
 ...
PMID:Dose response of alcohol-induced changes in BP, nitric oxide and antioxidants in rat plasma. 1568 47

Although moderate alcohol consumption seems to be protective against atherosclerosis, coronary artery disease rate increases with its higher doses. Platelet aggregation is an important process which contributes to the atherosclerosis. The aim of this study was to determine whether heavy ethanol consumption stimulates or inhibits platelet aggregation. Fourteen adult male Wistar rats were used. Ethanol (7.2%, v/v) in a modified liquid diet was given to eight rats for 21 days, which mimicked characteristics similar to human chronic alcoholism. Six rats constituted the control group. Adenosine diphophate (ADP) and collagen-induced platelet aggregation was measured in whole blood. We found reduced ADP-induced mean maximal aggregation in the alcoholic rat group compared to the control group at dose of 5 microM (p < 0.005). We also found decreased platelet aggregation responses to collagen in the alcoholic group (p < 0.006 for 2 microg/ml collagen, and p < 0.05 for 5 microg/ml collagen). In conclusion, chronic heavy ethanol consumption results in the decreased platelet aggregation in a rat model of alcoholism. Therefore, increased mortality from coronary artery disease in chronic alcoholism may be explained by other factors such as dietary imbalances and coexisting conditions, which include hypertension and depression.
 ...
PMID:Chronic heavy ethanol consumption is associated with decreased platelet aggregation in rats. 1588 63

There are many factors that contribute to hyperuricemia, including obesity, insulin resistance, alcohol consumption, diuretic use, hypertension, renal insufficiency, genetic makeup, etc. Of these, alcohol (ethanol) is the most important. Ethanol enhances adenine nucleotide degradation and increases lactic acid level in blood, leading to hyperuricemia. In beer, purines also contribute to an increase in plasma uric acid. Although rare, dehydration and ketoacidosis (due to ethanol ingestion) are associated with the ethanol-induced increase in serum uric acid levels. Ethanol also increases the plasma concentrations and urinary excretion of hypoxanthine and xanthine via the acceleration of adenine nucleotide degradation and a possible weak inhibition of xanthine dehydrogenase activity. Since many factors such as the ALDH2*1 gene and ADH2*2 gene, daily drinking habits, exercise, and dehydration enhance the increase in plasma concentration of uric acid induced by ethanol, it is important to pay attention to these factors, as well as ingested ethanol volume, type of alcoholic beverage, and the administration of anti-hyperuricemic agents, to prevent and treat ethanol-induced hyperuricemia.
 ...
PMID:Effect of ethanol on metabolism of purine bases (hypoxanthine, xanthine, and uric acid). 1593 2

Carbon disulfide exerted adverse effects on the structure or hemodynamics of the cardiovascular system, and whether ethanol exposure modifies the cardiovascular effect of carbon disulfide, was examined. Male Sprague-Dawley rats were used in the study. Animals in the control and ethanol groups drank water containing 5% sugar, or 10% ethanol in addition to 5% sugar, respectively, for 14 wk. Sepatare animals inhaled 700 mg/m3 of carbon disulfide for 6 h daily. Carbon disulfide treatment did not affect the food and fluid consumption of the animals, while this gas decreased body mass gain. CS2 increased arterial blood pressure and cardiac index, decreased their cardiac output, the fraction of the cardiac output, and blood flow for the kidneys and the lungs, and increased the relative heart, liver, and kidneys mass and the vascular resistance of the brain, lungs, and kidneys. Ethanol decreased the food and fluid consumption and body mass gain of the animals, the fraction of the cardiac output for the kidneys, and the vascular resistance of the liver, while it increased the blood flow of the brain and liver. Simultaneous administration of carbon disulfide and ethanol decreased the heart rate and increased the QRS duration. Significant interaction was found between the effect in case of heart rate, PQ distance, and QRS duration; carbon disulfide significantly increased the minimal-moderate effect of ethanol on all three parameters. With histological examinations no pathologic alterations were found in the organs studied. It was concluded that the early hemodynamic changes produced by carbon disulfide may play a significant role in the pathomechanism of the effects of the substance (hypertension, damage to the myocardium and kidneys). On the other hand, a potentiating interaction of carbon disulfide was expected with the effects of ethanol, at the administered concentration and dose in the study.
 ...
PMID:The effects of carbon disulfide and ethanol on the circulatory system of rats. 1602 Jan 77

Chronic ethanol intake and hypertension are related. In the present work, we investigated the effect of chronic ethanol (20% v/v) intake for 2, 6 and 10 weeks on basal arterial blood pressure, baroreflex and heart rate levels, as well as on the cardiovascular responses to the infusion of vasoactive agents in unanesthetized rats. Mild hypertension was observed after 2 weeks, 6 weeks or 10 weeks of treatment. On the other hand, no changes were observed in heart rate after long-term ethanol intake. Similar baroreflex changes were observed in 2- or 6-week ethanol-treated rats, and affected all parameters of baroreflex sigmoid curves, when compared to the control group. These changes were characterized by an enhanced baroreflex sympathetic component and a reduction in the baroreflex parasympathetic component. No differences in baroreflex parameters were observed in 10-week ethanol-treated animals. The pressor effects of i.v. phenylephrine were enhanced in 2-week ethanol-treated rats; not affected in 6-week treated animals and reduced in 10-week ethanol-treated rats, when compared to respective control and isocaloric groups. The hypotensive response to i.v. sodium nitroprusside (SNP) was enhanced at all different times of treatment, when compared to respective control and isocaloric groups. In conclusion, the present findings showed increased arterial pressure in the early phase of chronic ethanol consumption, which was consequent of rise in both systolic and diastolic pressures. Ethanol intake affected both the sympathetic and the parasympathetic components of the baroreflex. Vascular responsiveness to the pressor agent phenylephrine was initially enhanced and later on decreased during chronic ethanol intake. Vascular responsiveness to the depressor agent SNP was enhanced during chronic ethanol intake.
 ...
PMID:Chronic ethanol consumption alters cardiovascular functions in conscious rats. 1628 25

Alcohol-induced hypertension is well recognized with clear evidence for a direct pressor effect of chronic alcohol consumption provided by a number of intervention studies in humans. In experimental animals, the effect of alcohol on blood pressure is less consistent; however, in Sprague-Dawley rats, alcohol feeding consistently induces a hypertensive response. The mechanism of alcohol-induced hypertension is not clearly understood. Ethanol is known to induce certain cytochrome P450 (CYP) enzymes, particularly the 2E1 isoform, which has been shown to metabolise arachidonic acid (AA) to the 19-hydroxy metabolite (19-HETE), which could have pro-hypertensive activity; CYP4A, by comparison, is the principal AA omega-hydroxylase in the liver. Polyphenolic compounds, such as flavonoids, have been shown to inhibit some CYPs. 2. In this study, we determined the effect of alcohol administration on blood pressure and CYP-dependent AA metabolism in the rat and its possible modulation by red wine polyphenols. 3. Thirty male Sprague-Dawley rats were randomly allocated to three groups, which received water, low-dose ethanol (5% v/v) or red wine (diluted to contain 5% ethanol) for a period of 9 weeks. Bodyweight and blood pressure were measured weekly and 24h urine collected at baseline and every 2 weeks. Animals were killed at 9 weeks and blood and tissue samples were collected. The blood pressure of rats fed with alcohol increased significantly over the period of the study compared with controls (P<0.001). The blood pressure of animals fed 5% alcohol in the form of red wine was not significantly different from controls over the study period. The urinary excretion of 20-HETE did not differ significantly among the treatment groups over the study period and there was no effect of any treatment on the metabolism of AA by renal microsomes. Red wine, but not administration of the relatively low dose of alcohol alone, increased the expression of CYP2E1 protein in the liver and kidney and CYP4A in the kidney. Both red wine and alcohol decreased CYP4A protein levels in the liver compared with controls. 4. Our results suggest that constituents of red wine, possibly polyphenols, can attenuate the alcohol-induced rise in blood pressure in the Sprague-Dawley rat, although this effect does not appear to be mediated by the inhibition of CYP-derived AA metabolism.
 ...
PMID:Effect of alcohol on cytochrome p450 arachidonic acid metabolism and blood pressure in rats and its modulation by red wine polyphenolics. 1648 60

Low alcohol intake in humans lowers the risk of coronary heart disease and may lower blood pressure. In hypertension, insulin resistance with altered glucose metabolism leads to increased formation of aldehydes. We have shown that chronic low alcohol intake decreased systolic blood pressure (SBP) and tissue aldehyde conjugates in spontaneously hypertensive rats and demonstrated a strong link between elevated tissue aldehyde conjugates and hypertension in salt-induced hypertensive Wistar-Kyoto (WKY) rats. This study investigated the antihypertensive effect of chronic low alcohol consumption in high salt-treated WKY rats and its effect on tissue aldehyde conjugates, platelet cytosolic free calcium ([Ca2+]i, and renal vascular changes. Animals, aged 7 weeks, were divided into three groups of six animals each. The control group was given normal salt diet (0.7% NaCl) and regular drinking water; the high salt group was given a high salt diet (8% NaCl) and regular drinking water; the high salt + ethanol group was given a high salt diet and 0.25% ethanol in drinking water. After 10 weeks, SBP, platelet [Ca2+]i, and tissue aldehyde conjugates were significantly higher in rats in the high salt group as compared with controls. Animals on high salt diets also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidney. Ethanol supplementation prevented the increase in SBP and platelet [Ca2+]i and aldehyde conjugates in liver and aorta. Kidney aldehyde conjugates and renal vascular changes were attenuated. These results suggest that chronic low ethanol intake prevents salt-induced hypertension and attenuates renal vascular changes in WKY rats by preventing an increase in tissue aldehyde conjugates and cytosolic [Ca2+]i.
 ...
PMID:Low ethanol intake prevents salt-induced hypertension in WKY rats. 1668 63

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.
 ...
PMID:Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model. 1671 71

Ethanol is a molecule of enduring research interest because its consumption has important social as well as medical implications. With excessive ethanol consumption, there is higher prevalence for hypertension, stroke, cardiomyopathy, and arrhythmias. A principal mechanism by which ethanol exerts these cardiovascular effects is through modulation of blood pressure. In this article, we focus on recent research that pursues information on the effects of alcohol on blood pressure in human subjects, regardless of whether they have hypertension or not. Known means by which alcohol exerts hemodynamic effects are briefly covered, and insights on novel biomediators, such as endothelin and gene-based mechanisms, are presented. Newer tools, such as the Alcohol Use Disorders Identification Test-Consumption Questions (AUDIT-C) survey and carbohydrate-deficient transferrin (CDT) serum test, are also covered. Reducing excessive alcohol intake can produce a reduction in blood pressure of up to 4 mm Hg, on average, which could substantially affect the rates of stroke and ischemic heart disease.
 ...
PMID:Alcohol and its relationship to blood pressure. 1688 66

Low ethanol intake is known to have a beneficial effect on cardiovascular disease. In cardiovascular disease, insulin resistance leads to altered glucose and lipid metabolism resulting in an increased production of aldehydes, including methylglyoxal. Aldehydes react non-enzymatically with sulfhydryl and amino groups of proteins forming advanced glycation end products (AGEs), altering protein structure and function. These alterations cause endothelial dysfunction with increased cytosolic free calcium, peripheral vascular resistance, and blood pressure. AGEs produce atherogenic effects including oxidative stress, platelet adhesion, inflammation, smooth muscle cell proliferation and modification of lipoproteins. Low ethanol intake attenuates hypertension and atherosclerosis but the mechanism of this effect is not clear. Ethanol at low concentrations is metabolized by low Km alcohol dehydrogenase and aldehyde dehydrogenase, both reactions resulting in the production of reduced nicotinamide adenine dinucleotide (NADH). This creates a reductive environment, decreasing oxidative stress and secondary production of aldehydes through lipid peroxidation. NADH may also increase the tissue levels of the antioxidants cysteine and glutathione, which bind aldehydes and stimulate methylglyoxal catabolism. Low ethanol improves insulin resistance, increases high-density lipoprotein and stimulates activity of the antioxidant enzyme, paraoxonase. In conclusion, we suggest that chronic low ethanol intake confers its beneficial effect mainly through its ability to increase antioxidant capacity and lower AGEs.
 ...
PMID:Beneficial effect of low ethanol intake on the cardiovascular system: possible biochemical mechanisms. 1732 32


<< Previous 1 2 3 4 5 6 7 Next >>