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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cross-sectional survey of 5147 Australians attending a health screening clinic was conducted to determine if there was an association between habitual consumption of caffeine, or particular caffeine-containing beverages, and blood pressure. The average caffeine consumption of the study population was 240 mg/day. Caffeine consumption within the last three hours was found to be associated with significantly higher mean systolic and diastolic blood pressure in both sexes after controlling for age, adiposity, first degree relatives with hypertension, serum cholesterol level, alcohol consumption and tobacco smoking. Mean systolic and diastolic blood pressures differed significantly by 4 mmHg and 2 mmHg respectively for both males and females between those who had consumed caffeine within the last three hours and those who had not consumed it within the last nine hours (p less than 0.01). Average caffeine consumption per day was not associated with blood pressure in either sex after controlling for time since caffeine consumption. Logistic regression analysis was used to estimate the relative risk of high blood pressure (treated and untreated) for the groups consuming and not consuming caffeine in the last three hours. This relative risk was significantly greater than unity in females only (p less than 0.05). After controlling for time since caffeine consumption, caffeine consumption per day was not associated with significantly increased risk of high blood pressure.
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PMID:Caffeine consumption and blood pressure: an epidemiological study. 326 Feb 26

This study examines the extent to which a set of 10 demographic, behavioral, and medical risk factors explain black/white differences in hypertension. Data are from a cross-sectional examination of San Francisco transit drivers aged 25-65 years surveyed during 1983-1985 as part of an occupational health study. The inherent restriction of the study population to bus drivers and the further restriction to males in this population (764 blacks and 224 whites) controlled for factors related to occupation and sex. Control of 10 additional potential risk factors, including age, education, body mass index, smoking, and intake of caffeine and alcohol was possible in the analytic phase of the study. The unadjusted prevalence of hypertension (systolic blood pressure greater than or equal to 140 mmHg, diastolic blood pressure greater than or equal to 90 mmHg, or current use of antihypertensive medications) was 36.1 per cent for black males compared with 30.8 per cent for white males. The greatest difference in prevalence was observed for black males aged 55-64 years, for whom the prevalence was 46 per cent higher than for white males the same age. Despite higher rates of hypertension, blacks in all age groups exhibited lower levels of most major risk factors for hypertension. As a result, the independent effect of race on hypertension was increased rather than attenuated when the 10 covariables were taken into account (odds ratio of 1.27 in the unadjusted analysis, increasing to 1.54 in the adjusted, multivariate analysis). That this set of risk factors did not explain the higher rates of hypertension among blacks suggests that racial differences may arise from as yet unrecognized environmental and/or individual factors. The results also indicate that the association between race and blood pressure may have been underestimated in past studies that have relied on unadjusted analyses, in which negative confounding or masking effects of covariables have not been considered.
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PMID:Heightened risk of hypertension among black males: the masking effects of covariables. 326 95

Initial reports indicated that caffeine has a pressor effect, raising the possibility that it might contribute to hypertension. However, further studies have demonstrated that caffeine does not produce a persistent increase in blood pressure. Individuals who do not regularly consume caffeine may experience a slight increase in blood pressure when they are exposed to caffeine, but tolerance develops rapidly and blood pressure returns to baseline.
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PMID:Effects of caffeine on blood pressure. 271 18

Caffeine is the most widely consumed drug in Western society. The intake of caffeine-containing beverages in many adults and children often reaches levels that can induce pharmacological effects. Ninety-nine percent of ingested caffeine is absorbed and distributed to all tissues and organs. The effects of caffeine intake differ greatly according to acute or chronic intake, level of intake, and the development of tolerance. Caffeine administered acutely to non-users or recent abstainers can induce hypertension, arrhythmias, altered myocardial function, increased plasma catecholamine levels, plasma renin activity, serum cholesterol levels, increased production of urine, gastric acid secretion, and alterations in mood and sleep patterns. Tolerance to chronic caffeine intake develops in most individuals, with the cessation of its effects on the renal system, the cardiovascular system, the gastrointestinal system and, to some extent, the central nervous system. Moderate caffeine consumers probably need to have little concern for the effect of caffeine intake on their health if their other life-style habits are also moderate.
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PMID:The effects of caffeine on various body systems: a review. 330 87

Separate and combined effects of caffeine and mental arithmetic stress on systolic blood pressure (SBP) and heart rate (HR) were assessed in a double-blind, placebo-controlled study. Thirty-six Chinese nationals, half with and half without a family history of hypertension, received either 0, 125, or 250 mg of caffeine in three separate experimental sessions, each preceded by a 12-hour abstention from caffeine consumption. Caffeine and mental stress elevated SBP, but caffeine did not potentiate the SBP response to mental stress. Caffeine did not affect HR. A positive family history of hypertension was associated with larger SBP elevations to the higher dose of caffeine. Family history of hypertension was associated with larger blood pressure elevations during mental stress, but only under conditions of high-level stimulation provided by the initial exposure to the stress. These results support previous findings of greater cardiovascular reactivity to laboratory stress in individuals at high risk for hypertension.
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PMID:Caffeine, mental stress, and risk for hypertension: a cross-cultural replication. 334 98

The relation between coffee consumption and serum cholesterol level was investigated in a group of 9,043 hypertensive adults who were in the Hypertension Detection and Follow-up Program. In this study, men and women aged 30-69 years at baseline (1973-1974) had their serum cholesterol level measured at the two-year examination (1975-1976). Information about coffee, tea, and cola consumption was also obtained at that time from a food frequency questionnaire. The relation of coffee consumption and serum cholesterol level with potentially confounding variables including age, race, sex, diuretic status, diastolic blood pressure, cigarette smoking, relative weight, physical activity, stress, and education level was examined. When these variables were entered into a multiple regression equation, a positive association with coffee consumption and serum cholesterol level (p less than 0.05) was present. There was no significant relation between serum cholesterol level and consumption of tea, cola, or decaffeinated coffee--the other major contributors of caffeine to the diet--or total caffeine intake. This study indicates a significant positive relation between coffee consumption and serum cholesterol level.
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PMID:Coffee consumption and serum cholesterol in the hypertension detection and follow-up program. 338 21

In the very rare cases where a pregnancy occurs during oral contraceptive (OC) use, the blame is usually laid against the patient for having forgotten to take the pill. Evidence has started to accumulate, however, to suggest that neither the patient nor the pill is at fault in some contraceptive failures. It may be because the patient is taking other medicines and these may be preventing the pill from suppressing ovulation. Most drug interactions reducing or negating contraceptive activity are due to concomitant use of drugs having microsomal enzyme-inducing activity (e.g., some antibiotics, especially rifampicin, and anticonvulsants, including phenobarbital, phenytoin, and primidone). Other antibiotics (e.g., tetracycline) may also interact by interruption of the enterohepatic circulation of contraceptive steroids. Less well appreciated, OC steroids may themselves modify the metabolism and pharmacological activity of various other drugs (e.g., anticoagulants, benzodiazepines, beta-blockers, caffeine, corticosteroids, and tricyclic antidepressants); in this respect the OCs are acting as enzyme inhibitors. Contraceptive steroids may also interact with drugs that cause enzyme inhibition and this delays the metabolism of the hormonal agents. Interactions of this type would be expected to potentiate, not repress the action of the contraceptive steroids. Therefore the effects of such interaction might be presented in terms of increased incidence of side effects, including water retention, diabetogenic effects, hypertension, and an increased risk of thromboembolic disorders. The spectrum of interactions with OCs is presented in 3 tables.
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PMID:Drug interactions with oral contraceptives. 351 41

Cafergot is a combination of ergotamine tartrate and caffeine and may cause symptoms of peripheral vascular insufficiency. Iatrogenic ergotism should be suspected in any patient exhibiting ischemic symptoms while receiving this medication. Progression to fulminant necrosis and gangrene can occur. Two cases are presented and the management reviewed. This effect of ergotamine tartrate and caffeine may be an idiosyncratic hypersensitivity reaction with therapeutic doses or may result from excessive medication. Iatrogenic ergotism occurs most often in women in their mid-thirties with migraine syndrome. By alpha-adrenergic agonism, as well as by possible interactions with prostaglandins, calcium, and serotonin, ergotamine causes vasoconstriction of both arteries and veins. The angiographic pattern of spasm, collateral formation, and intravascular thrombi is typical. Treatment of ergotism depends on the severity of the symptoms and the possibility of gangrene. Discontinuation of ergotamine, cigarette smoking, and caffeine may be all that is necessary in most patients. Nitroprusside is the drug of choice in the treatment of acute vascular insufficiency from ergotism, but in a less urgent situation, prazosin has also been effective. Intra-arterial balloon dilatation has also been helpful. Other forms of therapy have been supportive and the results inconsistent. Cafergot should be used with extreme caution in patients with renal or hepatic failure, peripheral vascular disease, or pregnancy. Relative contraindications include hypertension, ischemic heart disease, and Raynaud's phenomenon.
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PMID:Recognition and treatment of arterial insufficiency from cafergot. 372 91

We compared the abilities of the adenosine antagonists caffeine and 8-(p-sulfophenyl)theophylline (8-SPT) to block adenosine receptor-mediated hypotension and bradycardia in anesthetized rats. Few quantitative data exist concerning the amounts of caffeine needed to prevent the cardiovascular effects of physiologic plasma adenosine concentrations or concerning the site of action (central or peripheral) of such blockade. Thus, dose-response curves were constructed for the antagonism by caffeine or 8-SPT of the hypotension and bradycardia caused by infusing adenosine i.v. or by giving bolus i.v. injections of the adenosine analogs 2-chloroadenosine, R-phenylisopropyladenosine or N-ethylcarboxamidoadenosine. We also quantitated the suppression by caffeine or 8-SPT of the ability of adenosine to potentiate nicotine-induced hypertension and tachycardia. Caffeine (EC50 = 92 microM) and 8-SPT (EC50 = 48 microM) blocked the hypotension produced by elevating plasma adenosine levels from 1.22 to 1.74 microM. Similar drug doses were needed to inhibit the potentiation by adenosine of pressor and chronotropic responses to nicotine or to antagonize the hypotensive and negative chronotropic effects of 2-chloroadenosine, R-phenylisopropyladenosine and N-ethylcarboxamidoadenosine. As expected, neither caffeine nor 8-SPT demonstrated selectivity for A1 (predominating at the heart) vs. A2 (predominating at blood vessels) receptor subtypes. Administration of as much as 50 mg/kg i.p. of 8-SPT failed to produce detectable brain levels of the drug, demonstrating its failure to gain access to the central nervous system and indicating that the site at which the drug antagonizes the cardiovascular effects of adenosine is peripheral.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antagonism of the cardiovascular effects of adenosine by caffeine or 8-(p-sulfophenyl)theophylline. 380 7

The mechanisms by which caffeine typically elevates blood pressure (BP) in humans have not been previously examined using a placebo-controlled design. Accordingly, oral caffeine (3.3 mg/kg body weight, equivalent to 2 to 3 cups of coffee) was given on 2 days and a placebo was given on 1 day to 15 healthy young men using a double-blind, crossover procedure. All 3 test sessions were held during a week of caffeine abstinence. Multiple measurements were made on subjects at rest (baseline values) and over a 45-minute interval after ingestion of caffeine for BP, heart rate, systolic time intervals and thoracic impedance measures of ventricular function. Baseline measurements were highly reliable for each subject across all sessions and yielded means for placebo vs caffeine days that were not different. Caffeine increased systolic and diastolic BP (p less than 0.01) and decreased heart rate (p less than 0.05). The pressor effect was due to progressively increased systemic vascular resistance and resulted in greater stroke work (p less than 0.01). There was no indication that caffeine increased cardiac output or contractility. These actions of caffeine were replicable when each caffeine day was tested separately against the placebo day. These results suggest that caffeine use by persons with cardiovascular diseases should be examined to determine whether caffeine's enhancement of vascular resistance may contribute to systematic hypertension and/or create excessive demands for cardiac work.
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PMID:Effects of caffeine on vascular resistance, cardiac output and myocardial contractility in young men. 401 15


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