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Query: KEGG:D01453 (caffeine)
 21,611 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of kola nut chewing and the effects attributed to it are briefly reviewed. Except for a generalisation that its effects are probably due to its caffeine content, no attempts have been made to quantify its specific actions. Preliminary observations on the cardiovascular system of the cat show that aqueous extracts of the nut evoke a dose dependent differential response - the 8 - 9% hypertensive effect of 0.01 ug - 1mg/ml doses contrasting with the 18--71% hypotensive response of 10--1000mgs/ml doses. Adrenergic receptor blockade showed no significant alteration of the response. With larger doses a bradycardia developed and cardiac arrythmias were observed as a terminal event. These results are compatible with the action of xanthines on the heart and peripheral vasculature. The possible role of the habitually chewed kola nut in the pathophysiology of cardiovascular disease and its implications have been briefly discussed.
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PMID:Some preliminary observations on the effects of kola nut on the cardiovascular system. 75 53

The effects of coffee and caffeine on haemostatic variables are reviewed. The potential relationship between coffee and cardiovascular disease warrants the study of possible links between coffee and haemostasis. The presently available evidence in favour or against such an association, however, is not very convincing and sometimes even conflicting. The findings on fibrinogen level and platelet in vivo activation as measured by plasma beta-thromboglobulin, seem to be the most reliable. If anything, these reports indicate an unfavourable effect of coffee, i.e. coffee may enhance thrombotic tendencies. Before more definite conclusions on the interference of coffee use with the haemostatic system can be made, more data are needed. In particular, randomized studies of coffee and caffeine intake in humans are indicated to assess the impact and the potential significance of coffee in such quantities as are commonly used by millions of people.
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PMID:Coffee, caffeine and hemostasis: a review. 207 19

Some recent epidemiologic studies have reported a nonlinear dose-response in the relationship between coffee consumption and health risks, such that the risks increase disproportionately to the increase in dose. Assuming caffeine contributes to the adverse health effects of coffee, a possible explanation for the nonlinear dose-response relationship is dose-dependent metabolism of caffeine. We examined the hypothesis that under chronic dosing conditions the metabolism of caffeine is dose-dependent. Nine healthy subjects were given, in randomized 5-day treatment blocks, placebo, 4.2 (low) and 12 (high) mg/kg/day caffeine in decaffeinated coffee, in six divided doses spaced throughout the day. On the third day of each dosing period, 25 mg of stable-isotope labeled caffeine (2-13C, 1,3-15N2) was given intravenously. Clearance of labeled caffeine fell from 0.118 (placebo treatment) to 0.069 (low dose; p less than 0.005) and to 0.54 (high dose; p less than 0.001) L/hr/kg. The formation and metabolite clearances of paraxanthine, the major primary metabolite of caffeine, also decreased comparing the low and high doses (p less than 0.05). We conclude that caffeine metabolism is dose-dependent, resulting in nonlinear accumulation of methylxanthines in the body. Dose-dependent metabolism of caffeine may explain in part why people who drink large amounts of coffee are at greater risk for cardiovascular disease.
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PMID:Dose-dependency of caffeine metabolism with repeated dosing. 240 Nov 26

Although habitual caffeine users ingest the drug repeatedly throughout each day, the persistence of caffeine's known cardiovascular effects with such repeated use has not been investigated. Blood pressure and heart rate were measured under resting conditions in 10 healthy, male coffee or tea drinkers for 2 hours following a pretreatment dose of caffeine (125 mg) on two separate days after overnight abstinence. Either a second caffeine dose or placebo was administered and measurements continued for 1.5 hours. Compared to placebo, the second dose of caffeine produced significant increases in heart rate and diastolic and mean arterial, but not systolic, blood pressures. The results suggest that the cardiovascular effects of caffeine may persist throughout the day with repeated administration of moderate amounts of caffeine. Habitual caffeine use does not necessarily lead to complete tolerance, which suggests that caffeine's cardiovascular effects could contribute to an increased risk of cardiovascular disease.
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PMID:Persistent cardiovascular effects with repeated caffeine administration. 277 3

The effect of caffeine consumption on mortality was evaluated in a historical cohort study of 10,064 diagnosed hypertensive individuals participating in the Hypertension Detection and Follow-up Program from 1973 to 1979. Total caffeine intake level from beverages (coffee and tea) and certain medications, was estimated at the 1-year visit. No evidence was found supporting an association between increased level of caffeine consumption and increased all-cause mortality or cardiovascular disease mortality during the following 4 years. Cigarette smoking was significantly associated with mortality; the association being more pronounced among non- and low-caffeine consumers for all-cause mortality and among non-caffeine consumers for all cardiovascular mortality except cerebrovascular mortality.
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PMID:Mortality patterns among hypertensives by reported level of caffeine consumption. 304 18

Caffeine can produce a mild hypertensive effect for a few hours after use. Some epidemiological data relate chronic coffee intake to an increased risk of cardiovascular disease. We explored the possibility that a regular intake of caffeine-containing beverages (tea, coffee, cola) might produce a chronic increase in blood pressure and increase the likelihood of developing sustained hypertension. A random population survey of 2436 adults was made, with standardized blood pressure readings and a food-frequency questionnaire to determine the regular intake of various nutrients. We found evidence that caffeine intake was positively related to an increased diastolic blood pressure but the effect was small (less than 1 mmHg at usual caffeine intake). There was no evidence that a regular caffeine intake increases the risk of being classified as hypertensive.
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PMID:Caffeine-containing beverages and the prevalence of hypertension. 324 Dec 68

Caffeine use during exposure to mental stress is an extremely common occurrence. Because both have been shown to alter blood pressure (BP) and its underlying hemodynamic mechanisms, the potential exists for additive or even synergistic effects. Changes in heart rate, BP and noninvasive thoracic impedance measures of left ventricular function were examined in young men (ages 20 to 36) at rest and during a demanding behavioral task performed 40 minutes after predosing with caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) or placebo in a double-blind crossover design. All subjects were healthy young men without history of cardiovascular disease, regular use of nicotine, recreational or prescription drugs or caffeine intolerance. Caffeine abstinence was required for 12 hours before each test session. Systolic and diastolic BP were elevated by both caffeine and the behavioral task alone (p less than 0.01 for each); when combined, caffeine's pressor effects were additive to those of the behavioral task. However, caffeine's pressor effect was produced by different mechanisms depending on the behavioral state. Caffeine increased systemic vascular resistance (p less than 0.01) under resting conditions, but it enhanced cardiac output (p less than 0.01) during behavioral arousal associated with the task. The combined influence of caffeine and the task increased the number of men in whom peak systolic BP reached hypertensive levels, and also synergistically increased cardiac minute work (p less than 0.01) and the rate-pressure product estimate of myocardial oxygen demand (p less than 0.05). Implications of these findings are discussed for long standing theoretical disputes regarding caffeine, its health consequences, and for methodologic issues in behavioral and clinical studies.
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PMID:Effect of behavior state on caffeine's ability to alter blood pressure. 335 44

In a population-based study of 590 Rancho Bernardo, California men aged 30-79 years without a history of cardiovascular disease, and who were first surveyed in 1972-1974, current cigarette smokers had significantly higher mean endogenous androstenedione, estrone, and estradiol levels compared to nonsmokers. In the cigarette smokers, a dose-response relationship was apparent for these hormones with mean levels increasing with increasing reported cigarette consumption. These differences persisted after adjusting for age and body mass index, and were not accounted for by either caffeine or alcohol intake, or exercise habit. In a further 89 men with a history of cardiovascular disease, hormone levels were not significantly related to smoking habit. The higher endogenous estrogen levels in cigarette smokers may confound the interpretation of studies reporting higher estrogen levels in male myocardial infarction survivors compared to controls.
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PMID:Cigarette smoking and increased endogenous estrogen levels in men. 360 47

Male Sprague-Dawley rats were treated with phenacetin, phenazone or caffeine in the diet or with combinations of these chemicals for up to 117 weeks. Twenty of twenty-eight rats receiving caffeine only developed moderate to severe myocardial fibrosis compared with five control rats, in spite of the fact that the control rats had a sixteen weeks longer average life-span. Four caffeine-treated rats had histologic evidence of acute myocardial infarction which was not found in any of the other rats. Forty percent of the rats treated with caffeine only or with caffeine and phenacetin in combination were found to have periarteritis nodosa-like lesions in the mesenteric vessels. Seventy-nine percent of the rats treated with caffeine only and 52 percent of those treated with caffeine and phenacetin died from cardiovascular disease, compared with 17 percent among the control rats. Thus, long-term administration of caffeine to Sprague-Dawley rats is associated with markedly reduced life-span due to cardiovascular disease.
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PMID:Cardiovascular lesions in Sprague-Dawley rats induced by long-term treatment with caffeine. 611 96

Caffeine and psychologic stress have similar physiologic effects. Moderate doses of caffeine were found to elevate blood pressure in healthy, young males during periods of rest and stress. Blood pressure during stress was also significantly higher after caffeine had been consumed. The elevation of blood pressure due to caffeine appears to add to that elicited by stress. The implications of these results for prevention and treatment of cardiovascular disease are discussed.
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PMID:Caffeine and cardiovascular responses to stress. 663 7


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