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

We determined kinin-generating activity (kininogenase) in the thoracic aorta of spontaneously hypertensive rats (SHRs) at age 5 and 15 weeks and in appropriately age-matched Wistar-Kyoto (WKY) rats. Aorta homogenates were incubated with partially purified dog kininogen, and the resulting kinins were extracted with ethanol. The kinins were determined by a sensitive kinin radioimmunoassay (RIA). Kininogenase activity was expressed as mean +/- SEM, picogram kinin generated/mg x protein/h. Active kininogenase in SHR was approximately one-third in 5-week-old and about one-fifth in 15-week-old rats when compared with their normotensive controls. Total kininogenase activity in SHRs was approximately 80% and 58% of the normotensive controls at ages 5 weeks and 15 weeks, respectively. Active enzyme was 14% of the total in 5-week-old SHRs, and it was only 5% of the total in 15-week-old SHRs. It seems unlikely that the changes in kininogenase are secondary to hypertension because blood pressor is only marginally elevated at 5 weeks according to the literature. We hypothesize that genetic hypertensive rats may suffer from an inherent deficiency in the kininogenase activity of the vascular wall. The deficiency may also be in the mechanism of activation of precursor enzyme.
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PMID:Kininogenase of the aortic wall in spontaneously hypertensive rats. 128 21

Risk factors for the 12-year incidence of definite coronary heart disease (CHD) among 3440 men who were middle-aged (51 to 59 years old) and 1419 men who were elderly (65 to 74 years old) at baseline examination were examined for differences in predictive values in terms of both relative risk and attributable (excess) risk of the highest versus the lowest quartile or appropriate categories. In multivariate models using Cox life-table regression procedures, serum cholesterol level, cigarette smoking, systolic blood pressure, and history of treatment for diabetes were significant predictors of incident CHD for both age groups. Alcohol consumption when modeled as drinker versus nondrinker showed a protective effect in both younger and older men. There was no dose relationship, however, among elderly drinkers. While the relative risks for the variables studied were similar between the two age groups, the excess risk was typically between 1.5 to 2.0 times higher for the older than the middle-aged men. In contrast, the detrimental effect of adiposity as measured by body mass index appeared to decline after age 65 for both measures of risk. This may partly be attributed to diminished adiposity overall in the older age group. The implications of these results are that serum cholesterol level, smoking, hypertension, diabetes, and possibly alcohol consumption continue to be important predictors for CHD when measured after age 65, and that the public health impact of these risk factors, in terms of excess risk, may be more important in the elderly.
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PMID:Do coronary heart disease risk factors measured in the elderly have the same predictive roles as in the middle aged. Comparisons of relative and attributable risks. 134 78

The "transurethral resection of prostate" syndrome (TURPS) is the clinical manifestation of the resorption into the patient's body of a large amount of glycocolle-containing irrigating fluid used for this procedure. The full clinical picture, which is seldom seen, consists of dyspnoea, nausea, arterial hypertension, an increased central venous pressure, cerebral oedema, cardiogenic shock and renal failure. Improved surgical techniques, as well as incomplete and atypical forms of the syndrome could explain this low incidence. Absorption into the blood stream may be rapid, by way of the prostatic venous plexi, or slower, from the spaces around the prostate and under the peritoneum. The present-day pathophysiological theory explains this syndrome by an acute hyponatraemia, sometimes dissociated from the hypoosmolality, the toxicity of glycocolle, and the neurological effects of hyperammonemia. Acute hyponatraemia, with blood sodium concentrations below 115 to 120 mmol.l-1, should be considered as potentially serious. The different mechanisms involved may act alone or together, thus explaining that the minor forms of the syndrome mostly consist of a neurological picture. The emergency treatment depends on the natraemia. It includes diuretics and progressive reloading of the patient with sodium in case of severe hyponatraemia with seizures. The best prevention is a correct surgical indication and technique. The resection should not last for more than 90 to 120 min. The major problem remains the early diagnosis of TURPS. Carrying out this surgery under regional anaesthesia is helpful for this purpose, but, in the near future, the best means might be the monitoring of expired ethanol concentrations.
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PMID:[Prostate transurethral resection syndrome]. 150 91

The relationship between regular alcohol consumption and blood pressure elevation is now firmly established. Outstanding issues which will be discussed relate to the nature of the dose response curve, interactions between alcohol and other dietary and behavioural factors, mechanisms involved and the question of any protective influence of alcohol on atherosclerotic and ischaemic cardiovascular disease associated with hypertension. Alcohol is an important contributory to the prevalence of hypertension, and resistance to drug therapy in drinking communities. Heavy drinking and binge drinking increases the risk of stroke.
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PMID:Alcohol and hypertension. 154 Oct 32

"Job strain" (defined as high psychological demands and low decision latitude on the job) has been previously reported to be associated with increased risk of hypertension and increased left ventricular mass index (LVMI) in a case-control study of healthy employed men, aged 30-60 years, without evidence of coronary heart disease. We hypothesized that job strain would be associated with increased ambulatory blood pressure (AmBP). A total of 264 men at eight work sites wore an AmBP monitor for 24 hours on a working day. In an analysis of covariance model, job strain was associated with an increase in systolic AmBP of 6.8 mm Hg (p = 0.002) and diastolic AmBP of 2.8 mm Hg at work (p = 0.03) after adjusting for age, race, body mass index, Type A behavior, alcohol behavior, smoking, work site, 24-hour urine sodium, education, and physical demand level of the job. Alcohol use also had a significant effect on AmBP. However, among subjects not in high-strain jobs, alcohol had no apparent effect on AmBP at work. Instead, alcohol use and job strain interacted such that workers in high-strain jobs who drank regularly had significantly higher systolic AmBP at work (p = 0.007). Among the other risk factors, only age, body mass index, and smoking had significant effects on AmBP. Job strain also had significant effects on AmBP at home and during sleep as well as on LVMI.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 May
PMID:Relation between job strain, alcohol, and ambulatory blood pressure. 156 68

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

Hypertension is a well-known side effect of ciclosporin A (CsA). In the present study the mechanisms of vasoconstriction in renal vessels were examined in the isolated perfused rat kidney. Kidneys were perfused with constant flow at a temperature of 37 degrees C with Tyrode's solution equilibrated with 95% O2/5% CO2. CsA was dissolved in ethanol. 500 and 2000 ng/ml increased resistance of renal vessels by 0.97 +/- 0.55 x 10(5) and 2.29 +/- 1.33 x 10(5) dyn s cm-5, respectively (mean values +/- SD, n = 12). The vasoconstriction developed gradually over 4 min. The vasopressor effect of CsA was not changed by saralasin (10(-6) M), nifedipine (10(-6) M) and ketanserin (10(-6) M), but was completely blocked by phentolamine and prazosin (each 10(-6) M). CsA-induced vasoconstriction was not prevented by perfusion with Ca(2+)-free solution containing 2 mmol EGTA. Similarly, pretreatment with reserpine to deplete sympathetic nerve endings from catecholamines did not affect CsA-induced vasoconstriction. The findings suggest that CsA-induced vasoconstriction is mediated by stimulation of alpha 1-receptors. Ca2+ influx does not play a role for CsA-induced vasoconstriction. Prolonged perfusion of rat kidneys with the vehicle cremophor EL elicits an irreversible increase in perfusion pressure.
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PMID:Mechanisms of ciclosporin A-induced vasoconstriction in the isolated perfused rat kidney. 158 25

Cardiovascular complications are among the most common and dangerous complications of cocaine abuse, ranging from episodic arrhythmias to myocardial infarction, strokes, cardiomyopathy, and sudden death. The central nervous system-mediated action of cocaine triggers an increase in circulating catecholamines, resulting in arterial vasoconstriction, increase in myocardial oxygen demand, myocardial ischemia, tachycardia, and other arrhythmias. The peripheral cardiovascular action of cocaine involves the inhibition of reuptake of catecholamines at adrenergic nerve terminals, with local release of epinephrine, direct stimulation and vasospasm of the coronary arteries, coronary intimal hyperplasia, inhibition of baroreceptors, interference with the electrical conduction through the myocardium, and direct myocardial toxicity. The cardiovascular complications of cocaine include cardiac dysrhythmias and hypertension, acute myocardial infarction, myocarditis, infectious endocarditis, ventricular dysfunction, dilated cardiomyopathy, hypotensive shock, and cerebral strokes. Cocaine-related vascular changes in the pregnant woman and fetus have been related to an increased incidence of abortion, abruptio placentae, and congenital anomalies of the fetus.
Recent Dev Alcohol 1992
PMID:Cardiovascular complications of cocaine abuse. 158 6

The present study employed enzyme-immunoassay to examine the effect of ethanol on endothelin-1 and/or -2(ET1 + 2) release from human umbilical vein endothelial cells. Thirty minutes of exposure to ethanol increased the release of immunoreactive ET1 + 2 from cultured endothelial cells in a dose-dependent manner. However, ethanol at concentrations of less than 400 mM did not induce any LDH release from the endothelial cells. Trypan blue exclusion test revealed that 400 mM solution of ethanol decreased the cell viability to 7.7%. Thus, ethanol was found to directly stimulate ET1 + 2 release from cultured human umbilical vein endothelial cells. This reaction of vascular endothelial cells against ethanol may be related to ethanol-induced cardiovascular diseases such as hypertension, myocardial infarction and stroke, as well as fatal alcohol syndrome.
Alcohol Clin Exp Res 1992 Apr
PMID:Ethanol stimulates immunoreactive endothelin-1 and -2 release from cultured human umbilical vein endothelial cells. 159 May 57

The role of alcohol as a risk factor for cerebral infarction and hemorrhage has been assesed in 200 middle-aged and elderly stroke patients and 200 controls matched for age, sex and hospital admission date. Computed tomographic brain scans were done in all but 10 of the stroke patients. Alcohol intake was reckoned on the 12 months preceding hospitalization and expressed in grams daily according to a standard nomogram. The Michigan Alcoholism Screening Test was used for the diagnosis of alcoholism. Cerebral infarction was present in 59% of the stroke patients and cerebral hemorrhage in 9%. The role of alcohol as risk factor for stroke proved to be small (Odds Ratio 1.86) and was practically lost after adjustment for the most common risk factors for cerebrovascular disorders (previous strokes, arterial hypertension, diabetes, obesity and hyperlipidemia). Our findings seem to suggest that alcohol is not an independent risk factor for stroke in the middle-aged and elderly. The data are, however, preliminary and are discussed in the light of methological problems.
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PMID:Cerebrovascular disorders and alcohol intake: preliminary results of a case-control study. 162 76


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