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)

Increased alcohol consumption causes hypertension and leads to higher death rates by hemorrhagic strokes. About half of the Japanese population have inactive low Km aldehyde dehydrogenase (ALDH2), which metabolizes acetaldehyde to acetic acid at very low concentrations, leading to severe pharmacological effects of aldehyde when drinking alcohol. We determined persons with inactive ALDH2 using a ethanol patch test. All male workers (n + 163), aged from 21 to 62 years in one factory in Japan took part. They were divided into two groups by alcohol consumption (nondrinkers, light drinkers of < 32 ml/l ethanol per day and moderate to heavy drinkers of > or = 32 ml ethanol per day). The prevalence of persons with inactive ALDH2 was 52.1%. The prevalence of moderate to heavy drinkers among persons with inactive ALDH2 was significantly lower than that among those with active ALDH2 (23% and 41%, respectively: P < 0.05). No significant differences of BP were observed between ALDH2 inactive and active groups at the same consumption of alcohol. This study showed a significant relationship between categories of alcohol use and SBP and DBP (P < 0.05, respectively) controlled for age and body mass index. The mechanism by which alcohol use elevates BP is unlikely to be related to the inactive ALDH2. However, inactive ALDH2 may act as a protective factor against hypertension by reducing alcohol consumption.
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PMID:Low-Km aldehyde dehydrogenase deficiency does not influence the elevation of blood pressure by alcohol. 800 21

Adenosine mechanisms are altered in brain stem nuclei associated with cardiovascular control in spontaneously hypertensive rats (SHR). Therefore, in the present study we used a number of techniques to compare the binding of the adenosine transport inhibitor [3H]nitrobenzylthioinosine ([3H]NBMPR) as well as adenosine deaminase immunoreactivity (ADA-IR) in brain stems and nodose ganglia of SHR and age-matched normotensive Donryu rats (DRY). Saturation binding revealed a single class of [3H]NBMPR binding sites in the dorsal brain stem of both strains, with Kd and Bmax values of 65 +/- 9 pmol/L and 282 +/- 31 fmol/mg protein, respectively, in SHR and 129 +/- 2 pmol/L and 217 +/- 23 fmol/mg protein in DRY. The Kd for [3H]NBMPR was significantly lower in SHR than in DRY. In competition assays, NBMPR, dilazep, dipyridamole, and adenosine displaced [3H]NBMPR binding, with Kd values of 0.21 +/- 0.04, 57.16 +/- 16.20, 1340 +/- 100, and 87000 +/- 12500 nmol/L, respectively, in DRY and 0.17 +/- 0.04, 28.24 +/- 3.60, 621 +/- 100, and 32000 +/- 6820 in SHR. Kd values for all displacers were lower in SHR; however, only values for dipyridamole and adenosine reached statistical significance. Autoradiography of adenosine transport sites with [3H]NBMPR revealed that unilateral nodose ganglionectomy reduced [3H]NBMPR binding on the denervated side of the nucleus tractus solitarius by 20.6 +/- 1.1% in DRY and 18.7 +/- 2.3% in SHR. The density of [3H]NBMPR binding in nodose ganglia was significantly lower in SHR (0.99 +/- 0.06 Bq/mm2) than in DRY (1.25 +/- 0.08). Immunohistochemical studies demonstrated ADA-IR in the dorsal vagal complex, associated with both nerve cells and fibers. Measurement of ADA-IR in the dorsal vagal complex with an 125I-labeled secondary antibody revealed a significantly higher level of ADA-IR in SHR (122%) than in DRY. In the nodose ganglia, ADA-IR was associated with a population of vagal perikarya. The present study helps provide a molecular explanation for the previously reported impaired cardiovascular responses to intra-nucleus tractus solitarius microinjection of adenosine in hypertensive rats.
Hypertension 1996 Dec
PMID:Markers of adenosine removal in normotensive and hypertensive rat nervous tissue. 895 92

A case control study on male primary hepatocellular carcinoma(HCC) and hepatitis B or C virus and some potential risk factors, e.g. blood transfusion, aldehyde dehydrogenase 2(ALDH2) genotype and drinking habits, was performed using two controls, i.e. a hospital control(HC) and a community control(CC) in Fukuoka and Saga Prefectures. Cases were obtained from the Second Department of Internal Medicine, Kurume University Hospital. The HCs were obtained from inpatients of two general hospitals in Kurume and the CCs were randomly sampled from the Kurume citizens being matched with age and sex to each case. Based on the HCs, odds ratios(ORs) of developing male HCC were statistically significant due to HBsAg or anti-HCV antibody positive status. Some discrepancies were observed between the two controls, i.e. higher proportions of past histories of diabetes or hypertension, of ALDH2 typical homozygote(ALDH2(1)/ALDH2(1)), and of heavy drinkers among the HCs, suggesting slight deviation of the HCs from the CCs in alcohol related aspects. Although ORs regarding accumulated amount of alcohol intake by age 40 based on the HCs were insignificant, two of the three corresponding ORs based on the CCs were statistically significant. Judging from alcohol related aspects between the two controls, the ORs for alcohol based on the HCs seems to be underestimated.
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PMID:A case-control study on male hepatocellular carcinoma based on hospital and community controls. 957 88

The characteristics of alcohol-induced flushing response were studied in some Siberian Native populations (Chukchi, Eskimo, Jakuts, Udege, and Nanaian). Flushing peculiarities were estimated and the interrelationship with drinking patterns, the ethanol patch test (EPT), and somatic disorders were analyzed. Frequency of flushing response varied from 9.0% to 66.7%, and was more often apparent among females. Only the Nanaian demonstrated typical flushing, which did not allow them to consume high doses of alcohol. In the rest of the populations flushing was "atypical," i.e., appearing sometimes after high doses of alcohol but not interrupting alcohol drinking, and not associated with a positive EPT. Direct genotyping in DNA samples of Chukotka Natives did not reveal atypical allele aldehyde dehydrogenase (AIDH 2/2). Frequencies of alcohol problems, alcohol dependence symptoms, and somatic disorders (arterial hypertension, silent ischemia, diffuse liver lesions, and noncalculous cholecystitis) were higher among atypical flushers compared to nonflushers (p < 0.05-0.01). The mechanism of the observed atypical flushing response is unknown. We speculate on its hereditary nature, since flushing alcoholics, compared to nonflushers, reported that their parents had flushing responses significantly more often. Further studies are required.
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PMID:Flushing response and its role in alcohol disease in Siberian populations. 1009 24

Taurine is known to lower blood pressure in essential hypertension and some experimental hypertensive models. Taurine has also been reported to activate aldehyde dehydrogenase and to inhibit the elevation of plasma acetaldehyde concentration after ethanol intake. Because acetaldehyde, the first metabolite of ethanol, is suspected to be responsible for many adverse effects of alcohol consumption, we examined the effect of taurine supplementation on ethanol-induced hypertension and abnormalities in the intracellular cation metabolism in Witar-Kyoto rats. In Study 1, systolic blood pressure and intraplatelet free calcium were significantly higher in rats who received 15% ethanol in drinking water than in control rats. Oral taurine supplementation (1% taurine and 15% ethanol in drinking water) completely prevented the development of ethanol-induced hypertension. Intraerythrocyte sodium and intraplatelet free calcium were significantly decreased in taurine-supplemented rats as compared with rats who received 15% ethanol only. In Study 2, hemoglobin-associated acetaldehyde (HbAA) was measured as a marker of protein-bound acetaldehyde. HbAA was significantly elevated in rats who received 5% ethanol in drinking water as compared with control rats. Taurine supplementation (1% taurine and 5% ethanol in drinking water) significantly decreased HbAA. Our findings suggest that the oral supplementation of taurine prevents ethanol-induced hypertension by decreasing protein bound acetaldehyde and altering the cation handling by the membrane.
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PMID:Oral taurine supplementation prevents the development of ethanol-induced hypertension in rats. 1082 Nov 39

To assess the usefulness of random capillary plasma glucose (RCPG) measurement in screening for diabetes mellitus in high-risk subjects, a RCPG measurement and a 75-g oral glucose tolerance test (OGTT) were performed in 684 women and 164 men, aged 16-76 years (mean+/-SD: 41.9+/-11.3 years). Risk factors included family history of diabetes in first degree relatives (53.8%), obesity (BMI > or =27 kg/m(2)) in 37.9%, dyslipidemia (78.4%), hypertension, i.e. BP > or =140/90 mmHg (28.5%), and history of gestational diabetes mellitus (16.6%). According to the 1997 ADA/1998 WHO Consultation criteria for a full OGTT, 118 cases (13.9%) were found to have diabetes. Each of 19 cases with RCPG > or =13.3 mmol/l had diabetes according to OGTT, 4.7% of 427 cases with RCPG<6.1 mmol/l had diabetes. Among 402 subjects with RCPG between 6.1 and <13.3 mmol/l, 19.7% were found to have diabetes. Thus, 446 (52.6%) of 848 subjects would have been saved from OGTT if RCPG was used as a screening test, in comparison to 33.1% if the cutpoints for RCPG (12.2 and 5.5 mmol/l) recommended by WHO Study Group (1985)/WHO Consultation (1998) were applied. Therefore, RCPG measurement is a useful screening test for the screening of diabetes mellitus in high-risk subjects.
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PMID:Random capillary plasma glucose measurement in the screening of diabetes mellitus in high-risk subjects in Thailand. 1116 92

Many previous experimental and epidemiological studies have shown that alcohol consumption has a positive correlation with the incidence of hypertension. The effects of ethanol on the nervous and vascular systems in relation to the mechanisms of alcohol-induced hypertension proposed so far are reviewed here. Alcohol ingestion influences many pathophysiological functions which regulate blood pressure, as follows: 1) Sympathetic nervous activity is increased after drinking. 2) Ethanol acts directly on the contractility of vascular smooth muscle. Ethanol acutely contracts some arteries and increases their contractile responses to agonists, while it also displays inhibitory effects on vasocontractility in other arteries. Thus, ethanol has two opposite actions, both of which depend on the kinds of vessels and animal species used for the experiments. Intra- and extracellular Ca2+ mobilization and activation of the contractile apparatus have been suggested as mechanisms for ethanol's vasocontractile actions. 3) Chronic alcohol ingestion has been reported to induce a deficiency of blood and intracellular magnesium, which influences cellular Ca2+ homeostasis through attenuation of plasmalemmal ATPase activity. Direct alcohol effects on cardiovascular systems may not be involved in hypertension that develops after long-term habitual drinking. 4) Ethanol affects vascular endothelial functions, inhibiting endothelial NO- and EDHF-dependent vasorelaxations. 5) The serum levels of vasoactive substances such as cathecolamines, renin-aldosterone, prostacyclin, and endothelin have been reported to be affected by alcohol ingestion or ethanol in vitro. 6) In heavy drinkers, alcohol withdrawal results in an elevation of blood pressure due to sympathetic nervous stimulation. 7) Long-term heavy drinking often results in the development of insulin resistance and glucose intolerance, which in turn triggers hypertension. 8) The difference in the genetic polymorphism of acetaldehyde dehydrogenase among Japanese people may not be directly related to development of alcohol-induced hypertension. As mentioned above, alcohol shows multiple actions on various factors regulating blood pressure. More detailed and integrated mechanisms for alcohol-induced hypertension, which is not a homogeneous disease, remain to be clarified.
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PMID:[Effects of ethanol on the nervous and vascular systems: the mechanisms of alcohol-induced hypertension]. 1126 32

In 1990-1992, a population-based study was carried out in the city of Oulu in northern Finland, to assess the prevalence of diabetes mellitus (DM) and impaired glucose tolerance (IGT) in a middle-aged population. We report the mortality of the study population until 31 December 1998. Altogether 831 subjects (82%) (369 men) participated in the baseline examinations, in which the prognostic risk factors were determined. Special attention was given to the effect of hyperglycemia on mortality. The WHO 1985, ADA 1997 and WHO 1999 criteria for diabetes, IGT and impaired fasting glucose (IFG) were used. Forty-one subjects (32 men) died during the average follow-up of 6.7 years, and the mortality rate was hence 7.7/1000 person-years. The results suggest that both fasting and post-load hyperglycemia are important predictors of mortality. Estimated by the Cox proportional hazards regression, the unadjusted hazard ratio (HR) for death was 2.5 (95% CI 0.9-6.6) in the subjects classified as diabetic according to the WHO 1999 criteria compared to normoglycemic subjects. The corresponding HR of the subjects with IFG was 2.5 (95% CI 0.7-8.8) and that of the subjects with IGT 1.5 (0.6-3.7). In addition, a high mortality was predicted by smoking (HR 4.2, 95% CI 2.0-8.8), male gender (HR 3.5, 95% CI 1.6-7.9) and hypertension (HR 2.3, 95% CI 1.1-5.1).
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PMID:Hyperglycemia as a risk factor of mortality in a middle-aged Finnish population. 1133 9

Taking into account all the risk factors and blood pressure levels, as indicated by several American and European recommendations available since 1997, is a leading strategy to reduce mortality and morbidity of hypertensive patients. The aim of this study was to quantify how, in 1999. French practitioners applied recommendations on hypertension (HTN), diabetes and hypercholesterolemia in recently diagnosed hypertensive patients and to evaluate whether or not the recommended targets were met. 1639 French GPs and cardiologists included 5831 recently diagnosed (7.5 +/- 3.6 months) hypertensives (57 +/- 12 years of age, M/F = 55/45%). Initial BP was 173 +/- 15/99 +/- 9 mmHg. 56% had no concomitant disease, 36% had either diabetes, dyslipidemia or coronary heart disease, 8% had at least two concomitant diseases. At the time of the study corresponding to 6.3 +/- 3.8 months after initiation of diet and/or medical treatment, their BP was 148 +/- 17/86 +/- 11 mmHg (-25/-19 mmHg). At that time only 37% of patients with stage 2 HTN were encouraged to adopt lifestyle modifications without any medical treatment as recommended by the JNC VI. Among these hypertensives, measurement of plasma cholesterol was performed in only 61%, HDL-C/LDL-C in 26% and blood glucose in 51%. In the patients with dyslipidemia, LDL-C was measured in only 47%. In the 677 diabetic patients only 27% had a glycated hemoglobin measurement. The percentage of patients reaching target BP was 59% as regard DBP < 90 mmHg, 25% as regard SBP < 140 mmHg, and 23% reached both target values of BP. In addition, 30% of patients with dyslipidemia reached the target LDL-C as defined by French recommendations (ANAES 1996) and 30% of the diabetic patients reached the target value for glycemia recommended by ADA (1997). In 1999 in France, a minority of patients reaches the national or international recommended target values for blood pressure, glycemia and plasma LDL-cholesterol. In spite of that, French practitioners do not implement all the available diagnostic tools to improve the treatment of metabolic disorders in hypertensive patients. As a conclusion, to improve the prognosis of hypertensive patients, it is mandatory to raise the awareness of physicians about multiple risk factor management and help them implement the recommendations in their daily practice.
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PMID:[Differences between management guidelines and global health strategies for arterial hypertension with metabolic disorders in France in 1999. Ohara study]. 1157 13

In Japanese and other Asians, the prevalence of genetically decreased mitochondrial aldehyde dehydrogenase (ALDH2) activity is higher than in Caucasians. The aim of this study was to elucidate the relation between ALDH2 genotypes and blood pressure levels or hypertension in Japanese. After obtaining informed consent for genetic analysis from 917 men and 1,478 women who lived in a mountainous farming region near Kyoto and who were free from cardiovascular disease and liver dysfunction, the authors identified the ALDH2 genotype in all subjects. Differences in blood pressure level among genotypes were then compared by analysis of covariance, and the relation between genotypes and hypertension was also analyzed by logistic regression analysis. The frequencies of genotypes *1/*1, *1/*2, and *2/*2 were 44.7%, 46.9% and 8.4% in men, and 50.1%, 43.2% and 6.8% in women, respectively. In men, systolic and diastolic blood pressures tended to decrease in the order of *1/*1>*1/*2>*2/*2. However, adjustment for confounding factors including alcohol consumption resulted in the disappearance of significance. Logistic regression analysis adjusted for the same confounding factors for men showed that the odds ratios (OR) of being hypertensive in the *2 allele to not having *2 allele were 0.67 (95% confidence interval (CI): 0.47-0.96). However, in the subgroup analyses, this relation was not observed in the group having a below-median level of alcohol consumption (OR = 0.92; 95% CI: 0.53-1.62) or in the group not taking antihypertensive agents (OR = 0.77; 95% CI: 0.52-1.15). Furthermore, we did not observe any relation between the ALDH2/*2 allele and hypertension in women (OR = 1.07; 95% CI: 0.80-1.42). The results suggest that there may be no causal relation between hypertension and the ALDH2 genotype per se, after excluding for some confounding factors, especially for alcohol drinking.
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PMID:Epidemiologic study of the association of low-Km mitochondrial acetaldehyde dehydrogenase genotypes with blood pressure level and the prevalence of hypertension in a general population. 1248 9


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