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)

This study examines the relationship of alcohol consumption and self-reported lifetime prevalence of hypertension among 19,284 non-institutionalized civilians in the United States. Cross-sectional data from the 1983 National Health Interview Survey, a national probability sample, were examined for each sex separately. Women who report hypertension consumed significantly less alcohol than women who did not report hypertension. Self-reported hypertensive men consumed equal or greater amounts of alcohol than self-reported normotensive men. Alcohol consumption was significantly associated with greater risk of hypertension among men, but not among women. After controlling for other risk factors significant effects for hypertension were found among males who on average consumed more than one drink/day. Beer consumption and spirits consumption above three drinks/day were significant predictors of male hypertension after adjustment for the confounding effects of other alcoholic beverage consumption and other risk factors. This study suggests that alcohol consumption by men who know that they are hypertensive is an important public health concern, with policy implications for targeting prevention efforts.
Drug Alcohol Depend 1990 Nov
PMID:Alcohol consumption, gender and self-reported hypertension. 226 91

Recent findings on the relation between alcohol abuse and ischaemic brain infarction are reviewed. Much of the association has hitherto been explained by the effects of confounding factors such as smoking. Alcohol increases blood pressure in both hypertensive and normotensive subjects and alcohol induced hypertension enhances the risk of both hemorrhagic and ischaemic strokes. Analysis of case histories shows that alcohol abuse has precipitated cerebral embolism in conjunction with cardiac diseases including alcoholic cardiomyopathy and paradoxical embolism due to deep vein thrombosis via atrial septal defect. Among young adults, falling when intoxicated with alcohol has caused traumatic dissection of the carotid artery and consequent brain infarction. Alcohol may predispose individuals to cerebral embolism, thrombosis and ischaemia via its effects on the coagulation cascade, platelet count and function and contractility of the cerebral vessels. Further studies are needed to prove that these mechanisms are significant and to identify any other mechanisms which may mediate the risk associated with alcohol abuse. On the basis of current data, alcohol should be considered as an independent risk factor for ischaemic cerebral infarction in young adults.
 ...
PMID:Alcohol abuse and brain infarction. 229 43

The relation of alcohol consumption to serum lipids and the severity of coronary atherosclerosis was examined in 212 men undergoing coronary angiography. The severity of coronary atherosclerosis was assessed in terms of the presence of greater than or equal to 75% diameter stenosis and the Gensini severity score. Alcohol consumption was divided into 4 categories: none (0 ml alcohol/week), light (1 to 100 ml alcohol/week), moderate (101 to 300 ml alcohol/week) and heavy (greater than or equal to 301 ml alcohol/week). Alcohol consumption was positively related to high-density lipoprotein cholesterol and inversely related to total cholesterol, but was not associated with triglyceride. After adjustment for these serum lipids as well as for cigarette smoking and systemic hypertension, the risk of coronary stenosis was significantly decreased in the moderate drinkers. A decreased risk among moderate drinkers also was noted in terms of Gensini's severity score. These findings suggest that moderate alcohol consumption may protect against severe coronary atherosclerosis.
 ...
PMID:Alcohol consumption, serum lipids and severity of angiographically determined coronary artery disease. 230 Dec 56

The purpose of this study was to investigate the effects of chronic ethanol consumption on blood pressure and vascular responses, specifically, the possible alterations in endothelium-dependent relaxation which are associated with ethanol-induced hypertension in the rat model. Male rats received ethanol in drinking water for 13 weeks. Systolic pressure was recorded weekly. Following treatment, segments of thoracic aorta with and without intact endothelium were used to generate relaxation-response curves to the endothelium-dependent agents, acetylcholine, ATP and bradykinin, as well as the endothelium-independent agents, adenosine and sodium nitroprusside. Mean systolic pressures at the end of the treatment period were: 127.8 +/- 1.2 and 151.1 +/- 1.3 mmHg for controls and ethanol-treated rats, respectively. Ethanol treatment did not affect the relaxation produced by either acetylcholine, ATP or sodium nitroprusside in aorta with or without endothelium. In contrast, ring segments with intact endothelium from ethanol-treated rats exhibited augmented relaxation in response to both adenosine and bradykinin compared to controls. Removal of the endothelium abolished the relaxation produced by bradykinin in both groups. Although removal of the endothelium had no effect on the relaxation produced by adenosine in the control group, it attenuated the adenosine-induced relaxation in the ethanol-treated group back to control levels. These data suggest that chronic ingestion of ethanol causes elevated blood pressure and augments the endothelium-dependent relaxation to bradykinin. These findings also suggest that chronic ethanol treatment can cause the appearance of an endothelium-dependent component in the relaxation produced by adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol
PMID:The effects of chronic ethanol treatment on endothelium-dependent responses in rat thoracic aorta. 232 85

We describe 3 patients with painful intraarticular knee effusions composed of a viscous milky white suspension of monosodium urate crystals, in the absence of any cellular component. Two patients presented with acute bilateral knee pain. One patient presented with unilateral knee pain of gradual onset. All 3 patients had a history of ethanol abuse. Two patients had a history of gout. Two patients had chronic renal insufficiency, hypertension, and congestive heart failure. One patient had alcoholic cirrhosis. Two patients' pain responded to colchicine. One patient's discomfort was relieved only by repeated arthrocentesis. We conclude that intraarticular free urate can cause painful joints in the absence of an apparent inflammatory response.
 ...
PMID:Intraarticular noninflammatory free urate suspension (urate milk) in 3 patients with painful joints. 235 87

The relationship between coronary risk factors and the severity of coronary artery stenosis (coronary score: CS) was estimated in 225 male subjects (aged 29-82 years, median 60 years old) who had undergone coronary arteriography for suspected coronary heart disease. CS was positively related to age, and levels of fasting blood sugar, uric acid, total cholesterol, low density lipoprotein cholesterol, and apolipoprotein B. Alcohol consumption, apolipoprotein AI and AII levels were inversely correlated to CS. Although, the level of CS was significantly higher in diabetics and hypertensives than in non-diabetics and non-hypertensives, the difference of CS level between diabetics and non-diabetics was more remarkable than that between hypertensives and non-hypertensives. Furthermore the ratio of Apo-B/Apo-AI was the most sensitive index of coronary artery stenosis rather than conventional atherogenic indices such as (TC-HDL-C)/HDL-C. Correlation between CS and the ratio of Apo-B/Apo-AI was positively and closely associated with aging, and this positive relationship was observed even in non-drinkers, heavier drinkers, non-diabetics and non-hypertensives. The reweighted least squares based on the least median of squares regression analysis indicated that about 27% of the variation in CS could be accounted for by age, complication of diabetes mellitus, complication of hypertension and the ratio of Apo-B/Apo-AI. These results indicate that the ratio of Apo-B/Apo-AI is a more sensitive parameter of the severity of coronary artery stenosis than any other atherogenic index. Further, aging, complication of diabetes mellitus, complication of hypertension and an increased level of the ratio of Apo-B/Apo-AI were responsible factors for the severity of coronary arteriosclerosis in male subjects.
 ...
PMID:[Clinical estimation of coronary risk factors with special reference to coronary arteriographic findings]. 238 94

The antihypertensive effect of calcium channel inhibitors (CCI) results mainly from their direct action on the vascular smooth muscle. However CCI may pass through the blood-brain barrier and may modulate central mechanisms involving calcium channels. Normotensive (WKY) and spontaneously hypertensive (SHR) (Okamoto) rats weighing 300 g were anaesthetized with pentobarbital (50 mg/kg i.p.) and ventilated. Mean arterial pressure (MAP) was measured from a catheter inserted into the femoral artery. Heart rate (HR) was electronically integrated. Vehicle (ethanol 95%), nifedipine and Bay k 8644 (Bay) were injected under a 1.5 microliter volume into the lateral ventricle of the brain (i.c.v.). Vehicle alone did not change significantly MAP or HR. The calcium-channel inhibitor nifedipine and the calcium-channel activator Bay had opposite effects, when i.c.v. injected: hypotension with bradycardia and hypertension without tachycardia, respectively. These effects are dose-dependent (5-50 micrograms/kg). They are of central origin since they are suppressed by ganglionic blockade by hexamethonium(100 mg/kg i.c.). Bilateral vagotomy suppressed the i.c.v.-nifedipine induced bradycardia. Previously i.c.v. administered nifedipine (5 micrograms/kg) suppressed the pressor response to Bay (5 micrograms/kg i.c.v.). Changes in MAP and HR are significantly more marked in SHR than in WKY. These results indicate that a calcium-channel inhibitor and a calcium-channel activator can modulate in opposite fashion central calcium-dependent mechanisms involved in blood pressure control.
 ...
PMID:[Central cardiovascular effects of a calcium inhibitor, nifedipine, and a calcium channel activator, Bay k 8644, in the anesthetized rat]. 243 47

The interaction of the vasoconstrictor peptide, endothelin-1 (ET-1), and the endothelium-derived vasodilator eicosanoid, prostacyclin, was examined as it pertains to the modulation of gastric mucosal integrity. Using an ex vivo chamber preparation of the rat stomach, the effects of intravenous ET-1 on the susceptibility of the mucosa to damage induced by topical application of an irritant, 20% ethanol, were examined. ET-1 significantly augmented gastric hemorrhagic damage induced by the irritant when administered at concentrations in the 10(-7) to 10(-6) M range. Pretreatment with indomethacin at a dose that inhibited gastric prostacyclin synthesis by over 85% resulted in significant augmentation of the ulcerogenic actions of ET-1. The damaging actions of ET-1 could be significantly reduced by topical pretreatment of the gastric mucosa with prostacyclin (5-50 micrograms/ml). This pretreatment also significantly reduced the hypertension and hemoconcentration observed following ET-1 administration. ET-1 also significantly augmented the susceptibility of the gastric mucosa to injury induced by hydrochloric acid. Oral administration of 150 mM HCl produced little or no gastric damage in control rats. However, a 5-min intravenous infusion of ET-1 produced significant increases in the severity of acid-induced gastric damage in a concentration-dependent manner (10(-7) to 10(-6) M). These results demonstrate that ET-1 is a potent ulcerogenic agent in the rat stomach. The ulcerogenic actions of ET-1 can be significantly reduced by prostacyclin, suggesting that the balance between endothelial cell release of ET-1 and prostacyclin may be an important factor in modulating gastric mucosal integrity.
 ...
PMID:The modulation of gastric mucosal integrity by endothelin-1 and prostacyclin. 247 84

The relationship between pancreatic duct pressure, duct permeability to macromolecules and the development of acute pancreatitis was studied in a cat model. Perfusion of the pancreatic duct with 15 mM glycodeoxycholic acid, ethanol administration, or secretagogue-stimulated pancreatic secretion against greater than 50 per cent duct obstruction resulted in an increase in peak pancreatic duct pressure in all animals. Duct permeability to 20,000 molecular weight dextran molecules was increased in 22 of 29 experimental animals compared with two of 22 control animals (P less than 0.01). Perfusion of the pancreatic duct with activated pancreatic enzymes resulted in acute pancreatitis in 24 of 29 experimental animals compared with three of 22 control animals (P less than 0.01). These results suggest that pancreatic ductal hypertension, resulting in increased ductal permeability to large molecules, may be a common early event in gallstone and alcoholic pancreatitis.
 ...
PMID:Pancreatic duct pressure, duct permeability and acute pancreatitis. 247

Plasma norepinephrine levels and alpha 2-adrenoceptor binding in central nervous system areas involved in blood pressure regulation were determined during the development of ethanol-induced hypertension in rats. Blood pressure was increased after the 4th week of ethanol feeding. Plasma norepinephrine levels of the ethanol-fed group were lower than those of the control group at most time periods studied even though blood pressure was elevated. 3H-Clonidine binding to alpha 2-adrenoceptors was decreased in the anterior and posterior hypothalamus of ethanol-fed rats throughout most of the study. Blood pressure in the ethanol-fed group was elevated when blood ethanol concentration was high, whereas blood pressure in this group was similar to that of the control group when blood ethanol concentration was low. Brain and plasma samples were taken during low blood ethanol which may explain the lack of positive findings. These results suggest that ethanol is a pressor agent and must be present to exert its cardiovascular effects. These findings suggest the importance of blood ethanol concentration at the time of study and also suggest that the blood pressure elevating effects of ethanol may be central rather than peripheral in origin.
Alcohol
PMID:Blood ethanol level and physiologic measurements during ethanol-induced hypertension. 254 Jul 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>