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Query: UMLS:C0085580 (essential hypertension)
 14,686 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.
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PMID:Hypertension risk and caffeine's effect on cardiovascular activity during mental stress in young men. 191 9

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

Weight reduction, alcohol restriction, mild salt restriction, eating a vegetarian diet and increasing aerobic exercise will generally lower the blood pressure in patients with essential hypertension. Eating a diet rich in potassium and reducing caffeine intake may also be helpful in reducing the pressure, but increasing the fiber or calcium intake will generally be ineffective. Reducing fat intake from the usual 40% of total calories to 25-30% may reduce hypertension directly or by weight reduction. Smoking, when combined with excessive caffeine or alcohol intake may have an additive effect on blood pressure. Monotherapy with such behavioral techniques as self-monitoring of blood pressure, biofeedback, meditation, yoga, progressive muscular relaxation or cognitive therapy may reduce the blood pressure to a variable degree, and combinations of these treatments may be even more successful.
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PMID:Non-pharmacological treatment of hypertension. 225 79

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)
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PMID:Caffeine may potentiate adrenocortical stress responses in hypertension-prone men. 254 9

The effects of guanabenz on serum lipids were assessed from data obtained in multicenter studies involving 483 patients treated for up to 2 years for essential hypertension. The mean age of the population was 50 years; 54% were male, and 61% were white. Dosage was titrated to maximize individual blood pressure response and was maintained at that level (mean final dosage 25 mg/day) for the remainder of the treatment period. After 4 weeks of treatment, mean total cholesterol levels decreased by 10 mg/dl (p less than 0.01), and the decrease was maintained throughout subsequent therapy. The decreases in cholesterol concentration were not affected by age, race, sex, previous diuretic therapy, previous antihypertensive therapy, smoking habits, or caffeine use. Complete lipid and lipoprotein profiles were obtained on serum specimens from 39 guanabenz-treated, overnight-fasted patients. Significant (p less than 0.01) mean decreases were observed for total cholesterol (-25 mg/dl) and low density lipoprotein cholesterol (-23 mg/dl) with no significant changes either in cholesterol levels of high density lipoproteins and very low density lipoproteins or in triglyceride levels. These changes indicate that guanabenz, given as monotherapy, has a favorable effect on the serum lipid profile with regard to cardiovascular risk.
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PMID:Effects of guanabenz on plasma lipid levels in hypertensive patients. 608 37

Resting and stimulated plasma noradrenaline and adrenaline concentration were compared in 45 females and 45 males of similar age who did not smoke, drink alcohol or caffeine-containing beverages. At rest plasma noradrenaline levels were consistently higher in females and adrenaline levels higher in males. These sex-related differences were maintained after isometric exercise, mental arithmetic and cold pressor testing. Resting noradrenaline concentration was negatively correlated with Quetelet index in males and positively correlated with age in females. These findings, based on precise catecholamine measurements under standardized conditions in subjects of similar age, reveal important sex-related differences which need to be taken into account in assessing sympatho-adrenal activity, particularly in relation to mechanisms in essential hypertension.
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PMID:Sex-related differences in resting and stimulated plasma noradrenaline and adrenaline. 646 38

Non-modulation has been proposed as an intermediate phenotype in human essential hypertension. The trait is characterized by blunted aldosterone and renal plasma flow responses to short-term angiotensin II (Ang II) infusion. Elevated tissue Ang II levels or decreased tissue adenosine levels could account for this decreased sensitivity to Ang II. In support of the latter possibility, endogenous adenosine has been shown to contribute to the renal vasoconstrictive response to Ang II in animals. We therefore tested the hypothesis that endogenous adenosine contributes to modulation of renal plasma flow in sodium-replete humans. We examined the effect of long-term administration of the adenosine receptor antagonist caffeine on baseline renal plasma flow and on the renal plasma flow response to short-term Ang II infusion in six salt-replete normotensive subjects in a single-blind, placebo-controlled study. para-Aminohippurate clearance was used to assess renal plasma flow. Ang II was infused in graded doses (0.3 to 3 ng/kg per minute) in the presence and absence of caffeine (250 mg PO TID for 7 days). Blood pressure, plasma renin activity, Ang II, electrolytes, and para-aminohippurate clearance were measured before and after each dose of Ang II. Caffeine did not alter either baseline blood pressure or the blood pressure response to Ang II but did increase baseline plasma renin activity from 0.72 +/- 0.09 to 1.42 +/- 0.26 ng angiotensin I/mL per hour (P = .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caffeine attenuates the renal vascular response to angiotensin II infusion. 824 16

A randomized, single-blind, controlled trial was conducted to examine the effects of guava fruit intake on BPs and blood lipids in patients with essential hypertension. Of 145 hypertensives that entered the trial, 72 patients were assigned to take a soluble fibre and a potassium-rich diet containing 0.5-1.0 kg of guava daily (group A) and 73 patients to their usual diet (group B), while salt, fat, cholesterol, caffeine and alcohol intake were similar in both groups. Mean age, mean body weight and male sex, were similar, and so were risk factors, mean BPs, mean serum sodium, potassium, calcium, magnesium, triglycerides, cholesterol and HDL-cholesterol in both groups. Dietary adherence to guava intake was checked by a questionnaire. After four weeks of follow-up on an increased consumption of dietary potassium and low sodium/potassium ratio, group A patients were associated with 7.5/8.5 mmHg net decrease in mean systolic and diastolic pressures compared with group B. Increased intake of soluble dietary fibre (47.8 +/- 11.5 vs. 9.5 +/- 0.85 g/day) was associated with a significant decrease in serum total cholesterol (7.9%), triglycerides (7.0%) and an insignificant increase in HDL-cholesterol (4.6%) with a mild increase in the ratio of total cholesterol/HDL-cholesterol in group A patients compared with group B. It is possible that an increased consumption of guava fruit can cause a substantial reduction in BPs and blood lipids with a lack of decrease in HDL-cholesterol due to its higher potassium and soluble fibre content, respectively.
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PMID:Can guava fruit intake decrease blood pressure and blood lipids? 838 69

Effects of caffeine on ambulatory blood pressure, heart rate, renin-angiotensin system, and ANP were studied in patients treated for mild to moderate hypertension in a randomized, double-blind, placebo-controlled, cross-over trial comparing 2 weeks of caffeine-free diet with 2 weeks of regular coffee use. Twenty-three patients (13 men; aged 28-74 years) with treated, mild to moderate essential hypertension and a regular intake of 3-4 cups of coffee daily completed the study. Mean 24-h, day- or night-time ambulatory blood pressure and heart rate were not different between regimens. Nor were there any effects on the renin-angiotensin system while ANP was significantly increased during caffeine intake. Compliance of the dietary regimen was excellent as assessed by serum caffeine concentration measurements. We conclude that habitual coffee drinking did not influence the 24-h blood pressure profiles or cardiovascular hormones in treated hypertensives.
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PMID:Effect of coffee on ambulatory blood pressure in patients with treated hypertension. 846 68


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