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)

Examined the cardiovascular effects of caffeine plus behavioral stress in men low versus high in risk of essential hypertension. Caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) or placebo was given on alternate days to 19 low-risk men (negative for parental hypertension and low-normal resting blood pressure, BP) and 20 high-risk men (positive history, high-normal BP). Forty minutes later, each worked for 15 min on a demanding psychomotor task during which BP, cardiac output, and vascular resistance were determined. During rest, caffeine raised vascular resistance in both groups. During the task, it supra-additively increased the systolic BP response by enhancing the rise in cardiac output, producing equivalent BP rises in both groups. Due to the higher resting pressures of the high-risk men, caffeine plus the task resulted in 50% of these having transient BP of 140/90 mg Hg or greater. Caffeine in combination with mental stress may produce undesirable BP in those at risk for hypertension.
 ...
PMID:Hypertension risk and caffeine's effect on cardiovascular activity during mental stress in young men. 191 9

Caffeine-induced blood pressure elevations are well documented in habitual consumers, occurring through both vasoconstrictive and cardiostimulatory actions. Whether caffeine hinders pressor regulation during exercise has been uncertain, particularly in those at risk for hypertension. Thus effects of caffeine versus placebo were studied during supine bicycle exercise in healthy men (ages 20 to 35). Hypertension risk was defined during screening: high risk (HRISK) = 135 to 154/85 to 94 mm Hg plus parental hypertension (n = 20); low risk (LRISK) = less than or equal to 132/84 mm Hg and no parental hypertension (n = 14). Exaggerated pressor responses (greater than or equal to 230/100 mm Hg) seen during exercise after placebo identified a subgroup of seven HRISKs indistinguishable at rest from the remaining HRISK men. This subgroup showed a larger resting diastolic response to caffeine (p less than 0.05) than LRISKs and other HRISKs. Compared with placebo, caffeine increased the number of LRISK (0% to 36%) and HRISK (35% to 50%) men reaching abnormal exercise blood pressures, and blunted normal increments in cardiac index at higher workloads among HRISK men (p = 0.05). Thus restriction of caffeine before exercise might benefit persons with either risk for hypertension or unusual sensitivity to caffeine.
 ...
PMID:Effects of caffeine on pressor regulation during rest and exercise in men at risk for hypertension. 192 62

The question of whether long-term elimination of coffee from the diet lowers blood pressure has not been settled. Consumption of Scandinavian-style "boiled coffee" is associated with coronary heart disease. However, little is known about the effect of brewing method on the blood pressure-raising potential of coffee. We have studied the effects on blood pressure and heart rate of total elimination of coffee and tea in comparison with drinking boiled coffee consumed as such, or boiled coffee consumed after filtration through paper filter. Thirty-one women and 33 men first consumed 6 cups/day of boiled and filtered coffee for 17 days. Then they were randomly divided into three groups, which for the next 79 days received either unfiltered boiled coffee (caffeine content 860 mg/l), boiled-and-filtered coffee (887 mg caffeine/l), or no coffee, the latter being replaced by fruit juice and mineral water. Total elimination of coffee did not significantly affect blood pressure or heart rate relative to boiled-and-filtered coffee. In subjects who drank boiled coffee, mean ambulant systolic blood pressure rose significantly relative to those who consumed boiled-and-filtered coffee (mean difference +/- SEM, 3.1 +/- 1.1 mm Hg, p = 0.006). This response showed a tendency to be stronger for women (4.5 +/- 1.8 mm Hg) than for men (1.7 +/- 1.2 mm Hg). We conclude that elimination of filtered coffee has no substantial long-term effect on blood pressure, but consumption of unfiltered boiled coffee may cause a slight but significant rise in systolic blood pressure.
Hypertension 1991 Nov
PMID:Boiled coffee and blood pressure. A 14-week controlled trial. 193 63

We studied caffeine- and noradrenaline-induced contraction in tail arteries from 4-week-old male SHR and age- and sex-matched WKY. After the sarcoplasmic reticulum Ca2+ had been depleted by the Ca(2+)-free EGTA (0.1 mmol/l) solution, the caffeine (10 mmol/l)-induced contractions in a low-Ca2+ (0.5 mmol/l) solution were smaller in SHR than in WKY. After the sarcoplasmic reticulum had been loaded with Ca2+ in physiological Ca2+ (2.5 mmol/l) solution, caffeine- and noradrenaline (10(-5) mol/l)-induced contractions in a Ca(2+)-free EGTA solution were smaller in SHR than in WKY. The Ca2+ concentration-tension relationship in skinned arterial fibres was similar in WKY and SHR. These data suggest that the ability of the sarcoplasmic reticulum to take up Ca2+ and store Ca2+ is decreased in SHR. The decreased take up and store of Ca2+ may increase cytosolic Ca2+, which elevates arterial resistance and develops hypertension in gene hypertension.
 ...
PMID:Abnormality in sarcoplasmic reticulum-dependent arterial contraction in responses to caffeine and noradrenaline in spontaneously hypertensive rats. 195 46

Previous studies strongly suggest that adenosine receptors on juxtaglomerular cells function to restrain the secretion of renin induced by a variety of stimuli. The clinical significance of this is that caffeine, a widely consumed adenosine receptor antagonist, could augment renin release responses to diseases such as renovascular hypertension, liver cirrhosis and heart failure and to therapeutic maneuvers such as salt restriction, diuretics and vasodilators. Caffeine may be particularly troublesome in this regard because this methylxanthine has central nervous system effects and intracellular actions that also might contribute to the overall ability of caffeine to potentiate renin secretion. The purpose of this study was to document the effects of caffeine on renin release responses to a vasodilator and to investigate what mechanisms were responsible for any augmentation of vasodilator-induced renin secretion. Accordingly, we compared the effects of caffeine vs. 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX; a xanthine that we documented in this study not to significantly enter the brain or penetrate cell membranes) on base-line and hydralazine-induced renin release in both normal and beta adrenoceptor-blocked (propranolol, 15 mg/kg) rats. Both xanthines (at a dose of 10 mg/kg plus 150 micrograms/min) attenuated adenosine-mediated hypotension and bradycardia, and DPSPX was at least as effective as caffeine in antagonizing peripheral adenosine receptors. Caffeine and DPSPX increased base-line plasma renin activity to a similar extent regardless of whether the animals were pretreated with propranolol. In rats with an intact beta adrenergic system, caffeine, but not DPSPX, increased the renin release response to low-dose hydralazine (1 mg/kg). Although both xanthines augmented the renin release response to high-dose hydralazine (10 mg/kg), caffeine was more efficacious in this regard. In beta adrenoceptor-blocked rats, neither caffeine nor DPSPX augmented the renin release response to low-dose hydralazine, whereas both xanthines equally potentiated the renin release response to high-dose hydralazine. These data demonstrate that caffeine increases base-line renin release primarily by blocking peripheral (most likely renal), cell-surface adenosine receptors; however, caffeine potentiates vasodilator-induced renin secretion in part by blocking peripheral (most likely renal), cell-surface adenosine receptors and in part by additional central nervous system and/or intracellular mechanism(s) that involve the beta adrenergic system.
 ...
PMID:Caffeine potentiates vasodilator-induced renin release. 200 84

The sympathetic nervous system may initiate or maintain hypertension, and a range of approaches that reduce sympathetic activity is often of value in management. These may include nonpharmacological methods, such as the various forms of behavioral therapy (e.g., meditation, relaxation, and biofeedback techniques); weight reduction and avoidance of particular foods and agents that stimulate sympathetic activity (including caffeine and alcohol), and regular physical exercise. Pharmacological therapy includes centrally acting drugs such as alpha-methyldopa, clonidine, and reserpine; ganglionic blockers such as hexamethonium; agents acting on sympathetic nerve terminals such as guanethidine and debrisoquine; and drugs that may act at multiple sites, such as the beta-adrenergic blockers. The role of reducing sympathetic activity in the current management of hypertension and its complications is considered in this overview.
Hypertension 1991 Apr
PMID:Management of hypertension by reduction in sympathetic activity. 201 96

The present study characterizes cellular calcium stores that are sensitive to norepinephrine and caffeine in arteries from deoxycorticosterone acetate hypertensive rats. Mesenteric arteries from normotensive and hypertensive rats were excised and cut into helical strips for isometric force recording. In calcium-free solution, phasic contractile responses to norepinephrine (5.9 x 10(-9) to 5.9 x 10(-6) M), but not caffeine (0.3-30 mM), were greater in hypertensive arteries. D-600, a calcium channel blocker, or removal of the endothelium did not alter phasic contractions to norepinephrine or caffeine. In contrast, contractions to both norepinephrine and caffeine were inhibited by ryanodine, a drug that depletes calcium from intracellular stores. An inhibitor of phospholipase C (2-nitro-4-carboxyphenyl N,N-diphenylcarbamate) attenuated contractions to norepinephrine but not those to caffeine. The augmented response to norepinephrine in hypertensive rats did not occur early after implantation of the mineralocorticoid, suggesting that this vascular change may not play a role in the development of high blood pressure in this experimental model. The augmented response to norepinephrine was reduced in mineralocorticoid-treated rats maintained on a low sodium diet, and these rats had blood pressures in the normotensive range. Because contractile responses to caffeine were not enhanced in arteries from hypertensive rats, we conclude that the cellular store for calcium is not enlarged compared with that in normotensive arteries. In contrast, the mobilization of calcium from cellular stores by norepinephrine is augmented in mineralocorticoid hypertension. This augmented response may be linked to altered phospholipase C activity and thus to an augmented action of inositol trisphosphate that releases calcium from intracellular sites.
Hypertension 1991 May
PMID:Agonist-sensitive calcium stores in arteries from steroid hypertensive rats. 202 5

The hypothesis of this study was that specific lifestyle patterns would be predictive of, or increase the risk for, uncontrolled hypertension in drug-treated hypertensive subjects. By means of a previously validated questionnaire, alcohol consumption, smoking, exercise, calcium intake, sodium intake, caffeine intake, body weight pattern and perceived stress level were evaluated in 364 subjects who attended a hypertension clinic in a large urban teaching hospital. The subjects were divided into controlled and uncontrolled categories on the basis of a clinic blood pressure reading. The number of prescribed drugs was not different between the two groups. Stratified analysis identified a high perceived stress level, a high calcium intake, and a lower body mass index as predictive of uncontrolled hypertension. Other variables showed no significant correlation. The conclusion of the study is that traditional risk factors for hypertension may assume less importance in drug-treated hypertensive patients than in untreated hypertensive patients.
 ...
PMID:Predicting success in antihypertensive drug therapy: the importance of nondrug variables. 202 85

Caffeine produces an acute increase in blood pressure in the research laboratory, but its effect on the ambulatory blood pressure during normal daily activities is unknown. In 25 normotensive, caffeine-naive subjects, daily administration of 400 mg caffeine produced a small increase (+3/+3 mm Hg, P less than .001) in ambulatory daytime blood pressure on the first day, with values returning to baseline by the third day. The initial rise in blood pressure was associated with a fall in heart rate (-3 beats/min, P less than .02). Readings taken the morning following the first day of caffeine ingestion did not show any persistent effect of caffeine on blood pressure. A 400 mg dose of caffeine causes a small increase in daytime ambulatory blood pressure, but tolerance develops with daily caffeine consumption. Infrequent ingestion of caffeine may cause a transient rise in blood pressure which is unlikely to be harmful to an individual but might influence the diagnosis of hypertension in a patient with a borderline elevated blood pressure.
 ...
PMID:The effect of caffeine on daytime ambulatory blood pressure. 842 69

Since the membrane Ca2+ handling properties of the arterial smooth muscle sarcoplasmic reticulum may be altered in genetic hypertension, we studied caffeine- and noradrenaline-induced contractions in tail arteries from spontaneously hypertensive rats (SHR) at the prehypertensive stage (4 weeks old) and from age-matched Wistar-Kyoto rats (WKY). After the sarcoplasmic reticulum had been loaded with Ca2+ by pretreatment with physiological Ca2+ solution, caffeine- and noradrenaline-induced contractions of the tail arteries, measured in a Ca2(+)-free solution [containing 0.1 mmol/l ethyleneglycol-bis-(beta-aminoethylether)-N,N,N',N'-tetraace tic acid], were smaller in SHR than in WKY. After caffeine-releasable Ca2+ in the sarcoplasmic reticulum had been depleted by pretreatment with the Ca2(+)-free solution, the caffeine-induced arterial contractions in a low-Ca2+ (0.5 mmol/l) solution were smaller in SHR than in WKY. The Ca2+ concentration-tension relationship in skinned arterial fibres was similar in WKY and SHR. These data suggest that the ability of the sarcoplasmic reticulum to take up and store caffeine- and noradrenaline-releasable Ca2+ is decreased in SHR. The development of hypertension in SHR may be explained by an impaired function of the sarcoplasmic reticulum in arterial smooth muscle.
 ...
PMID:Alteration in sarcoplasmic reticulum-dependent contraction of tail arteries in response to caffeine and noradrenaline in spontaneously hypertensive rats. 215 7


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