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

The effects of caffeine on aortic smooth muscle contractility during hypertension were studied in SHR and WKY control rats. To compare the effects of Mg++ on vascular reactivity induced by caffeine 1.2 mM MgCl2 was either included or omitted from the Krebs solution bathing the aortic tissue. The role of alpha-adrenergic receptors and verapamil-sensitive Ca++ channels in eliciting caffeine induced contraction in aortic tissues was also examined in Sprague Dawley rats. We report that the aortic smooth muscle from SHR animal was less responsive than WKY aortic smooth muscle to 10 and 20 mM concentrations of caffeine. Caffeine induced a relaxation of aortic smooth muscle contracted with 60 mM KCl or 10(-7) M NE. However, the relaxation response was slower in SHR as compared to WKY rats. To assess the involvement of alpha-adrenergic receptors in caffeine induced aortic contractility alpha 1- and alpha 2-receptors were blocked with 10(-7) M prazosin and 10(-7) M yohimbine respectively. The caffeine induced aortic contractility did not seem to involve alpha-adrenergic receptors. A blockade of verapamil sensitive Ca++ channels with 10(-7) M verapamil failed to inhibit caffeine induced aortic contractility. These results indicate that caffeine involves release of Ca++ in vascular muscle, however, Ca++ is released from a site other than the one controlled by alpha-adrenergic receptors. Also, the Ca++ channels involved are other than the Verapamil sensitive Ca++ channels. Yet it is clear that if the aortic contractility is due to Ca++ release alone, then caffeine is a potent agent for Ca++ release in the aortic smooth muscle of rat. Additionally, the caffeine-sensitive mechanism for aortic smooth muscle contraction is impaired during hypertension.
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PMID:In vitro caffeine induced aortic smooth muscle reactivity in rat. 233 85

Some of the critical links between sodium metabolism and vascular smooth muscle (VSM) contraction have been examined in an effort to explain the role of sodium in the etiology of hypertension. We found that the Na electrochemical gradient across the sarcolemma plays a critical role in the control of contractility in rat aorta and bovine tail artery. Reducing external Na and/or increasing internal Na increases vascular reactivity to norepinephrine (NE), to K and (in rat aorta) to caffeine, and slows relaxation; marked reduction in the Na gradient induces contraction. These effects appear to be the results of Ca movements mediated by Na/Ca exchange. Studies with Ca channel blockers and with alpha-adrenoceptor antagonists (except when NE was used) indicate that these effects cannot be attributed to Ca entry through Ca channels or to release of endogenous alpha-agonists. There is increasing evidence that individuals with essential hypertension have kidneys with an impaired ability to excrete Na. The retained Na (Cl) and attendant (slight) volume expansion may be compensated by the secretion of a (natriuretic) hormone which inhibits Na pumps. Inhibition of the Na pump in kidney tubules would be expected to induce a natriuresis (and net negative Na balance). Inhibition of the Na pump in VSM should increase intracellular Na, and thus enhance contractility via Na/Ca exchange. These mechanisms may explain the increased vascular reactivity and vascular tone that are the hallmark of essential hypertension and many other types of hypertension. The direct natriuretic action of the hormone, as well as the pressure natriuresis that results from its action on VSM, may help to protect these hypertensive individuals against the tendency to extracellular fluid volume expansion at the expense of the elevated blood pressure.
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PMID:Sodium metabolism and hypertension: how are they linked? 243 44

The effect of caffeine on blood cortisol levels and blood pressures was examined during rest and in response to a challenging psychomotor task in men with a low versus high risk of essential hypertension. Thirty-four healthy men ages 21-35 years were selected such that 17 were at high risk for hypertension (positive parental history and screening blood pressures of 135/85-155/95 mm Hg) and 17 were at low risk (negative parental history and no pressures above 132/84 mm Hg). Testing consisted of quiet rest (20 minutes); oral placebo (grapefruit juice) or caffeine administration (3.3 mg/kg in grapefruit juice); rest during a postdrug absorption period (40 minutes); work on an unsignalled simple reaction time task (15 minutes); and quiet rest (20 minutes). Blood pressures were recorded at 2-minute intervals, and blood samples were withdrawn via an indwelling catheter at the end of the baseline, drug absorption, task, and recovery periods. The combination of task plus caffeine produced the highest blood pressures in men at risk for hypertension. Cortisol levels were found to be sustained during rest in members of the high risk group after they had consumed caffeine, whereas members of the low risk group showed a modest decline. The high risk subjects also showed a significant rise in cortisol during (+3.7 micrograms/dl) and after (+4.0 micrograms/dl) work on the reaction time task after caffeine consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Aug
PMID:Caffeine may potentiate adrenocortical stress responses in hypertension-prone men. 254 9

In a previous study we discovered that the adenosine receptor antagonist, caffeine, increases plasma renin activity and blood pressure in renin-dependent renovascular hypertension. The purpose of the present investigation was to determine whether methylxanthines augment the increase in renin secretion induced by a reduction in renal perfusion pressure and, if so, whether this effect is mediated by a direct action on juxtaglomerular cells. Accordingly, we examined the effects of infusions of caffeine and theophylline directly into the renal artery on the increase in renin secretion induced by suprarenal aortic constriction. All studies were conducted in dogs receiving an intravenous infusion of propranolol to prevent changes in renin secretion mediated indirectly via the sympathetic nervous system. Caffeine (5 mg/min) increased the renin response to suprarenal aortic constriction about 10-fold without significantly affecting renal hemodynamics or excretory function. Theophylline (5 mg/kg), on the other hand, did not significantly increase the renin response to a reduction in renal perfusion pressure, but did increase urine flow and sodium excretion about 10-fold. However, in the non-filtering, beta-adrenoceptor blocked, canine kidney, theophylline markedly increased the renin response to suprarenal aortic constriction. These results indicate that methylxanthines can potentiate the renin response to a reduction in renal perfusion pressure most likely by directly affecting the juxtaglomerular cells; however, since increased sodium delivery to the macula densa inhibits renin release, the extent to which methylxanthines affect the renin response to renal artery hypotension depends on how vigorous the diuretic response is to a given methylxanthine.
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PMID:Methylxanthines augment the renin response to suprarenal-aortic constriction. 257 Mar 68

The purpose of this study was to examine the effects of caffeine and psychological stress on systolic blood pressure (SBP) and heart rate (HR) in 40 healthy Black and White male regular coffee drinkers. Half the subjects had a positive family history of hypertension (FH+), and half did not. The effects of 250 mg of caffeine versus placebo (3 mg) in decaffeinated coffee were compared in a within-subject, double-blind, cross-over design. SBP and HR were measured at rest, after caffeine ingestion, during mental arithmetic stress, and during recovery. Results confirmed previous findings with White men that a moderate dose of caffeine produced significant increases in SBP and little effect on HR and that the pressor effects of caffeine and stress combined additively. Contrary to expectations, no overall race or family history differences in SBP levels or in SBP reactivity were observed. FH+ Blacks, however, evidenced slower SBP recovery than Whites. Whites evidenced higher overall HR levels than blacks, but this difference was not specific to caffeine or to mental stress. Mechanisms of racial differences in reactivity underlying differential risk for hypertension are discussed, as well as the utility of caffeine as a pharmacologic probe for such differences.
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PMID:Impact of caffeine and psychological stress on blood pressure in black and white men. 263 Feb 95

Forty-eight healthy, young, normotensive black and white women, half with and half without a parental history of hypertension, were studied using a double-blind, randomized design. Systolic (SBP) and diastolic (DBP) blood pressures and heart rate (HR) were recorded in response to 250 mg of caffeine vs placebo (3 mg) during rest and during a stressful mental arithmetic task. Results indicated no racial or parental history differences in response to caffeine or to stress. Surprisingly, our female subjects evidenced a small drop in SBP (1 mm Hg) and a decline in HR (5 bpm), and, as expected, they demonstrated a rise in DBP of 6 mm Hg in response to caffeine. The effects of caffeine on SBP and HR were contingent on the experimental condition such that the difference in SBP and HR between the high vs low dose of caffeine was significant only under the caffeine plus psychological stress condition. These effects were only partially consistent with those previously observed in males. Previous evidence of significantly greater DBP pressor effects when caffeine is consumed under stressful conditions was confirmed. However, in this study, the caffeine alone condition had little effect on SBP reactivity and promoted a decrease in HR reactivity. The results are discussed in relation to previous research on males, and recommendations for future research are offered.
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PMID:Cardiovascular reactivity with caffeine and stress in black and white normotensive females. 267 65

It has been known for several years that blood pressure in the elderly may fall after a meal. Although the mechanism is not fully understood, postprandial blood pressure reduction seems to be related to glucose related factors, since blood pressure only falls after oral glucose loading, but not after oral fructose, fat or protein loading. Vasoactive gastrointestinal hormones may play a role in the glucose induced vasodilation of splanchnic vasculature, but attempts to identify such hormones were unsuccessful. Therefore we suggest that interference of insulin with a sympathetic response diminished by age or disease to splanchnic vasodilation, may be responsible for the postprandial fall in blood pressure in the elderly. However, vasodilator effects of insulin or a baroreflex response diminished by insulin do not seem to be involved. Although the clinical significance of postprandial blood pressure reduction remains uncertain, several advises can been given. Treatment of hypertension, small carbohydrate meals, use of caffeine before a meal or treatment with the somatostatin analogue SMS 201-995 may have a beneficial effect.
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PMID:[Reduction in blood pressure after meals in the elderly. A review article]. 267 21

The effect of decaffeinated versus regular coffee on blood pressure and heart rate was investigated. In a randomized double-blind, crossover trial, 45 healthy volunteers (23 women and 22 men, 25-45 years old) with a habitual intake of 4-6 cups coffee/day received 5 cups of regular coffee each day for a period of 6 weeks, and 5 cups of decaffeinated coffee for the next 6 weeks or vice versa. The background diet was kept constant. The total amount of caffeine ingested was 40 mg during the decaffeinated coffee period and 445 mg during the regular coffee period. Use of decaffeinated coffee led to a significant but small decrease in systolic (mean +/- SEM, -1.5 +/- 0.4 mm Hg; p = 0.002) and diastolic (-1.0 +/- 0.4 mm Hg; p = 0.017) ambulant blood pressure and to a small increase in ambulant heart rate (+1.3 +/- 0.6 beats/min; p = 0.031). Individual differences in rate of caffeine metabolism did not explain differences in long-term response of blood pressure to caffeine. We conclude that in normotensive adults replacement of regular by decaffeinated coffee leads to a real but small fall in blood pressure. However, it remains to be established whether a mass switch from regular to decaffeinated coffee would significantly reduce the total incidence of hypertension-related disorders.
Hypertension 1989 Nov
PMID:Effect of decaffeinated versus regular coffee on blood pressure. A 12-week, double-blind trial. 268 Sep 64

Since the early 1900s, coffee has been implicated as having adverse effects on human health. Recent attention has focused on coffee's relation to CHD, but because of conflicting results of epidemiologic studies on coffee and CHD mortality, attention has turned to the effects of coffee and caffeine on individual CHD risk factors. Coffee's effect on serum lipids does not appear to be due to caffeine. If in fact an adverse effect on lipids exists, it may be related to other factors including biochemical constituents other than caffeine, hardness of the water used in preparation, and the method of preparation, filtered coffee having no effect. The data are fairly convincing that chronic coffee ingestion does not induce hypertension, although acute consumption produces a small, short-lived increase in BP. The least well understood effect of coffee is its potential to induce cardiac arrhythmias, including potentially lethal ventricular ectopy in certain individuals. More work is needed in this area of arrhythmias before any concrete recommendations can be made. Until more convincing evidence against coffee is compiled, it appears that, at least in moderate amounts in otherwise healthy persons, coffee is a safe beverage.
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PMID:Coffee and coronary heart disease: a review. 268 80

We compared sodium-calcium (Na-Ca) exchange in vascular smooth muscle between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Aortic rings of 11 SHR and 11 WKY rats aged 11-12 weeks were superfused with physiological saline, and isometric tension was measured. Systolic blood pressure was higher in SHR (174 +/- 12 mm Hg) than in WKY rats (132 +/- 4 mm Hg): 1) In the presence of 10 microM phentolamine, 10 microM verapamil, and 5 mM caffeine, reduction of ionized extracellular sodium concentration [( Na+]o) from normal (139.2 mM) to 1.2 mM (replaced by N-methyl-D-glucamine) caused an external Ca2+-dependent increase in tonic tension (calcium entry by Na-Ca exchange). The rate of increase was higher in SHR (35.4 +/- 3.9 mg/min) than in WKY rats (17.9 +/- 1.3 mg/min) (p less than 0.01). 2) In the presence of phentolamine, verapamil, and caffeine, relaxation from low-Na+ contraction was promoted by external calcium removal. The rate of relaxation was directly related to [Na+]o. The rates of relaxation at normal (139.2 mM) [Na+]o were higher in SHR than in WKY rats (p less than 0.05). The rates of relaxation at 1.2 mM [Na+]o (calcium extrusion by adenosine triphosphate-driven calcium pump) were not different between SHR (11.6 +/- 2.8 mg/min) and WKY rats (8.9 +/- 2.5 mg/min). The increase in the rates of relaxation from 1.2 mM to normal (139.2 mM) [Na+]o (calcium extrusion by Na-Ca exchange) was greater in SHR (34.9 +/- 6.6 mg/min) than in WKY rats (17.1 +/- 4.5 mg/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jun
PMID:Increased sodium-calcium exchange in arterial smooth muscle of spontaneously hypertensive rats. 273 27


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