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

Caffeine is known to raise blood pressure (BP). We examined a single oral dose of caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) on BP in 18 hypertensive (HTN) and 12 age-matched, normotensive (NT) men for 3 h. Systolic BPs were significantly higher after caffeine for both groups (P < .001) for the entire 3 h. The HTN group showed persistent elevation in diastolic BP for 3 h, whereas the increment of diastolic BP became smaller in the NT group 90 min after caffeine ingestion. Our results suggest that caffeine consumption may affect both diagnosis and treatment of hypertension and abstinence from caffeine may be beneficial, especially for hypertensive individuals.
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PMID:Prolonged increase in blood pressure by a single oral dose of caffeine in mildly hypertensive men. 798 67

Current medical practice recommends the use of alternatives to estrogen-replacement therapy for the treatment of menopausal sequelae in younger women with breast cancer, although this clinical recommendation is undergoing reappraisal. Until prospective randomized studies addressing hormone use in this population are available, estrogen use in breast cancer patients will remain controversial. Because estrogen-replacement therapy is not the standard of practice and there is limited information available on nonestrogen therapies, women with breast cancer who are menopausal may not be prescribed or counseled about nonestrogen options. The efficacy, safety, and extent of use of most nonestrogen treatment modalities (other hormonal preparations, nonhormonal drugs, homeopathic preparations, and non-drug treatments) are not well documented and, unlike estrogen, many are selective in their benefit and do not share estrogen's universal impact. The use of several nonestrogen approaches for the prevention and treatment of osteoporosis has been promising. Traditional recommendations to maintain skeletal integrity, such as weight-bearing exercise; a diet rich in calcium and limited in caffeine, alcohol, and protein; avoidance of smoking; and measures to minimize trauma have been expanded to include the use or investigation of drugs (either alone or in combination). These drugs include progestins, vitamin D metabolites, injectable and intranasal synthetic salmon calcitonin, bisphosphonates, sodium fluoride, parathyroid hormone, growth factors, tamoxifen, etc. Strict control of the known risk factors, such as smoking, dyslipidemia, and hypertension as well as exercise, weight control, and the use of tamoxifen, are employed for the prevention and treatment of cardiovascular complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonhormonal alternatives for the management of early menopause in younger women with breast cancer. 799 60

Coffee is the most commonly used drug in the United States. The medical literature is conflicted regarding the harmful effects of coffee and caffeine. Because the articles that have appeared are so different, a formal meta-analysis is not the ideal way to summarize the data. However, this literature review suggests that coffee does not have an appreciable effect on hyperlipidemia, hypertension, ischemic heart disease, or cancer. The effects of decaffeinated coffee are much less well-defined, and there is little rationale for recommending that patients switch to decaffeinated coffee. A less appreciated problem with caffeine is that it may increase the risk of osteoporosis and hip fracture.
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PMID:Coffee: brew or bane? 801 Mar 38

A 27 year-old deeply unconscious male patient with shallow spontaneous respiration was admitted to hospital following an epileptoid convulsion with a tentative diagnosis of cerebral trauma. On admission he was noted to have hyperpyrexia, tachycardia and hypertension. The clinical and laboratory findings pointed to intoxication. Aspiration of the stomach produced a large amount of coffee grounds, but not tablets or other poison. The plasma caffeine level was 29 micrograms/ml, which is potentially lethal. Therapy was commenced with a beta-blocker, an anticonvulsive drug and an antipyretic, and supportive symptomatic measures were undertaken. After 12 hours the patient was fully conscious, orientated and cooperative. He subsequently admitted having ingested about 500 g ground coffee with the intention of obtained a "high" state of drug intoxication, which he had successfully achieved on previous occasions with a smaller amount of coffee and without complications. The clinical picture was consistent with the expected signs of caffeine intoxication whereby the central effects of the substance remain to be clarified. This appears to be the first report of caffeine misused in this manner. In cases of intoxication with convulsions of uncertain aetiology, caffeine poisoning should be considered in the differential diagnosis.
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PMID:[Life-threatening caffeine poisoning by using coffee as a psychoactive drug]. 805 4

beta-Adrenergic blocking agents are of therapeutic value in the treatment of migraine and various cardiovascular disorders (angina pectoris, cardiac arrhythmia, hypertension). Owing to their sedative effect, they are also used as doping agents in sport. A characteristic feature of beta-blockers is the alkanolamine side-chain terminating in a secondary amino group. The pKa values vary from 9.2 to 9.8. Because some beta-blockers are hydrophilic and some lipophilic, simultaneous determination is difficult. In this work, a method based on micellar electrokinetic capillary chromatography (MECC) was developed for the separation and determination of beta-blockers. The 0.08 M phosphate buffer (pH 7.0) solution contained 10 mM N-cetyl-N,N,N-trimethylammonium bromide (CTAB). Ten parent beta-blockers in human urine could be separated in a single run and determined quantitatively by the internal standard (2,6-dimethylphenol) method. Neither endogenous compounds in urine nor caffeine and its metabolites interfered with the analysis. The clean-up procedure for urine consisted of a simple filtration through 0.5-microns PTFE membranes. The MECC method exhibited good repeatability and a linear range of 25-150 micrograms/ml. The method was applied to determination of oxprenolol in real samples.
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PMID:Determination of ten beta-blockers in urine by micellar electrokinetic capillary chromatography. 809 37

Chronic parenteral administration of ouabain to normal rats raises plasma ouabain concentrations to low nanomolar levels and induces hypertension [C. M. Yuan, P. Manunta, J. M. Hamlyn, S. W. Chen, E. Bohen, J. Yeun, F. J. Haddy, and M. B. Pamnani. Hypertension 22: 178-187, 1993 and see also M. P. Blaustein. Am. J. Physiol. 264 (Cell Physiol. 33): C1367-C1387, 1993]. To determine whether rat arteries are sensitive to these low ouabain levels, we tested the effects of various ouabain concentrations on caffeine-evoked contractions (CEC) in rat aortic and small mesenteric artery rings. CEC amplitude was used as a measure of the sarcoplasmic reticulum (SR) Ca2+ content. Ouabain increased CEC in aortic as well as mesenteric artery rings, but the effects in the aorta were difficult to quantitate because the CEC were often oscillatory. Mesenteric artery, under control conditions and after sensitization with 10-30 nM phenylephrine (PE), exhibited biphasic ouabain dose-CEC response curves. Low concentrations of ouabain (0.1-10 nM) caused small significant increases in CEC, but a further effect was observed only with > or = 10 microM ouabain. PE shifted the ouabain dose-response curve toward lower ouabain concentrations; conversely, ouabain shifted the PE dose-response curve toward lower PE concentrations. It appears that nanomolar concentrations of ouabain can influence vascular responsiveness to vasoconstrictors. We conclude that rat vascular smooth muscle contains both high- and low-affinity ouabain receptors, possibly corresponding to Na+ pumps with alpha 3- and alpha 1-subunit isoforms, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nanomolar ouabain augments caffeine-evoked contractions in rat arteries. 823 91

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)
Hypertension 1993 Dec
PMID:Caffeine attenuates the renal vascular response to angiotensin II infusion. 824 16

The present study was aimed to determine the effect of caffeine on the development of renal hypertension. Two-kidney, 1-clip (2K1C) hypertension and deoxycorticosterone acetate (DOCA, 200 mg/kg, subcutaneous implantation)-salt (0.9% NaCl drinking) hypertension were instituted in Sprague-Dawley rats. They were then grouped into two groups each: one was supplemented with caffeine (0.1%) in their drinking solution and the other was not. Systolic blood pressure was measured up to 24 days. Caffeine exacerbated the development of 2K1C hypertension in association with a higher plasma renin concentration (PRC). Caffeine ingestion, however, did not exacerbate but ameliorated DOCA-salt hypertension in which PRC was comparable between the caffeine-ingested and control groups. Concentrations of plasma atrial natriuretic peptide (pANP) were significantly different between the caffeine-ingested and control groups neither in 2K1C nor in DOCA-salt rats, suggesting that ANP was not responsible for the modified blood pressure. Acute caffeine infusion (350 micrograms/min, 30 min) in anesthetized normotensive rats caused increases in urinary excretion (volume and sodium) and in PRC without significantly affecting the blood pressure and pANP. These results suggest that caffeine specifically exacerbates 2K1C hypertension through increasing renin release whereas it ameliorates DOCA-salt hypertension possibly through increasing renal excretion.
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PMID:Chronic caffeine ingestion exacerbates 2-kidney, 1-clip hypertension and ameliorates deoxycorticosterone acetate-salt hypertension in rats. 830 20

Cardiovascular diseases are the most important cause of mortality in industrialised countries. Contrary to cancer research, cardiovascular research mostly ignores toxic effects, apart from nicotine, caffeine, alcohol, a few pharmaceutical drugs, and the (in our countries) minor workplace problems carbon disulfide, nitrate esters, and carbon monoxide. But many workplace chemicals are known to be harmful to the cardiovascular system; beside the mentioned, also organic solvents, metals, pesticides, vinyl chloride, polychlorinated biphenyls, etc. Several toxic mechanisms in the cardiovascular system are already known: e.g., long-term development of atherosclerosis, hypertension, coronary heart disease, cardiomyopathy, and arrhythmia. To neglect cardiovascular toxicity is contrary to logic; for many cardiovascular diseases toxic effects may be constitutive; more of these effects may be seen in the future.
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PMID:[Do workplace chemicals harm the heart?]. 832 24

Intracellular free Mg2+ concentration ([Mg2+]i) has been implicated in the pathogenesis of hypertension. It has been postulated that Mg2+ through its antagonistic effects on intracellular Ca2+ concentration may affect tension and contractility of vascular smooth muscle cells. An established cell line of rat thoracic aorta cells (A10) was cultured on glass cover slips, and [Mg2+]i was determined by fluorescent techniques on single cells with the use of mag-fura-2. Basal [Mg2+]i was 0.52 +/- 0.02 mM (n = 15). Vascular smooth muscle cells were challenged with A23187 plus 5 mM MgCl2 to rapidly elevate [Mg2+]i. [Mg2+]i increased to a peak of 1.03 +/- 0.09 mM within 1-2 s and then quickly declined to below basal levels, 0.30 +/- 0.03 mM, within 45-60 s despite the continued presence of A23187 and external Mg2+. The rapid removal of the Mg2+ challenge to below basal levels suggests the presence of intracellular transport mechanisms, likely in intracellular compartments or organelles. Spatial imaging studies indicated that Mg2+ is heterogeneously distributed within the cell with the greatest variations in the perinuclear region, the area of most cytosolic organelles. Vanadate, an inhibitor of P-type adenosinetriphosphatases, inhibited the removal rate from 10.2 +/- 0.9 to 6.8 +/- 1.0 microM/s. Inhibitors of intracellular Ca2+ mobilization, thapsigargin, dantrolene, and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester, inhibited Mg2+ sequestration. Ryanodine and caffeine had no effect on Mg2+ removal. Ruthenium red did not inhibit Mg2+ sequestration, but oligomycin B slowed its removal. These studies demonstrated that [Mg2+]i in vascular smooth muscle cells is carefully controlled by active mechanisms involving intracellular and plasma membrane transporters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dynamics of intracellular free Mg2+ changes in a vascular smooth muscle cell line. 834 44


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