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Hypertension Causes

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34761. Sleep apnea causes daytime hypertension. (PubMed)

Sleep apnea causes daytime hypertension. 9011562 1997 02 06 2016 11 24 0021-9738 99 1 1997 Jan 01 The Journal of clinical investigation J. Clin. Invest. Sleep apnea causes daytime hypertension. 1-2 Dempsey J A JA eng Editorial Comment United States J Clin Invest 7802877 0021-9738 AIM IM J Clin Invest. 1997 Jan 1;99(1):106-9 9011563 Animals Blood Pressure physiology Dogs Humans Hypertension complications diagnosis etiology Hypoxia etiology Rats Respiration Sleep Apnea Syndromes complications

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1997 Journal of Clinical Investigation

34762. Smoking and stroke: a causative role : Heavy smokers with hypertension benefit most from stopping  (PubMed)

Smoking and stroke: a causative role : Heavy smokers with hypertension benefit most from stopping  9765161 1998 11 06 2018 11 13 0959-8138 317 7164 1998 Oct 10 BMJ (Clinical research ed.) BMJ Smoking and stroke: a causative role. Heavy smokers with hypertension benefit most from stopping. 962-3 Aldoori M I MI Rahman S H SH eng Editorial England BMJ 8900488 0959-8138 AIM IM Cerebrovascular Disorders etiology Humans Hypertension complications Risk Factors Smoking adverse effects 1998 10 9 1998

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1998 BMJ : British Medical Journal

34763. Familial Primary Pulmonary Hypertension (Gene PPH1) Is Caused by Mutations in the Bone Morphogenetic Protein Receptor–II Gene (PubMed)

Familial Primary Pulmonary Hypertension (Gene PPH1) Is Caused by Mutations in the Bone Morphogenetic Protein Receptor–II Gene Familial primary pulmonary hypertension is a rare autosomal dominant disorder that has reduced penetrance and that has been mapped to a 3-cM region on chromosome 2q33 (locus PPH1). The phenotype is characterized by monoclonal plexiform lesions of proliferating endothelial cells in pulmonary arterioles. These lesions lead to elevated pulmonary-artery pressures, right (...) -ventricular failure, and death. Although primary pulmonary hypertension is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs, including phentermine-fenfluramine. We genotyped 35 multiplex families with the disorder, using 27 microsatellite markers; we constructed disease haplotypes; and we looked for evidence of haplotype sharing across families, using the program TRANSMIT. Suggestive evidence of sharing was observed with markers

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2000 American Journal of Human Genetics

34764. The causes of essential hypertension. (PubMed)

The causes of essential hypertension. 1. Confusion between the criteria for defining and diagnosing hypertension may have misled the search for the causes of hypertension. 2. The systematic approach of molecular genetics appears to offer the best chance of explaining hypertension, but the attractions are partly offset by the large numbers required, and unproven record of the genetic techniques in finding functional mutations in complex human disorders. 3. Part of the evidence for the polygenic (...) that several more single-gene disorders causing hypertension will be found. The sibships where all members are hypertensive are inconsistent with the segregation of Mendelian genetics and suggest the selection of some genes linked to hypertension at the time of gamete maturation.

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1996 British journal of clinical pharmacology

34765. Nicardipine does not cause deterioration of glucose homoeostasis in man: a placebo controlled study in elderly hypertensives with and without diabetes mellitus. (PubMed)

Nicardipine does not cause deterioration of glucose homoeostasis in man: a placebo controlled study in elderly hypertensives with and without diabetes mellitus. The effect of the calcium antagonist nicardipine on insulin secretion and glucose homoeostasis was investigated in elderly hypertensives with and without diabetes mellitus; 15 patients with essential hypertension for at least 10 years and normal glucose tolerance according to standard criteria (Group I) and 15 elderly hypertensive (...) by haemoglobin Alc and fructosamine, nor did it significantly affect the plasma insulin response either to glucose or arginine in Groups 1 and 2. Only the glucagon response to arginine was significantly reduced in diabetic hypertensives. Small, non-significant variations in the metabolic and hormonal parameters were seen in additional two groups of patients (Groups 3 and 4), matched with Groups 1 and 2 for age, sex and diseases, who took capsules containing placebo. Thus, nicardipine did not produce any

1992 European journal of clinical pharmacology

34766. Thioguanine used in maintenance therapy of chronic myeloid leukaemia causes non-cirrhotic portal hypertension. Results from MRC CML. II. Trial comparing busulphan with busulphan and thioguanine. (PubMed)

Thioguanine used in maintenance therapy of chronic myeloid leukaemia causes non-cirrhotic portal hypertension. Results from MRC CML. II. Trial comparing busulphan with busulphan and thioguanine. Portal hypertension with varices developed in 18/675 patients with chronic myeloid leukaemia (CML) in a randomized trial comparing busulphan with busulphan and thioguanine. All 18 had received the drug combination and none busulphan alone (P less than 0.0001). Ascites was also seen significantly more (...) often in the combination arm (P less than 0.05). These results strongly suggest that the addition of thioguanine was responsible for the development of portal hypertension. The histological features were predominantly those of non-cirrhotic portal hypertension--either idiopathic portal hypertension with minimal morphological abnormalities, nodular regenerative hyperplasia or in two cases leukaemic infiltration only was noted. Cirrhosis was present in 3/16 cases studied. Both treatment groups

1991 British journal of haematology

34767. Potassium chloride lowers blood pressure and causes natriuresis in older patients with hypertension. (PubMed)

Potassium chloride lowers blood pressure and causes natriuresis in older patients with hypertension. Epidemiologic surveys, experimental studies in animals, and clinical trials in young and middle-aged patients with hypertension indicate that dietary potassium lowers blood pressure. The mechanism of the antihypertensive effect is not well defined. Variations in serum potassium within the physiologic range may directly affect vascular smooth muscle tone. Potassium may also influence

1992 Journal of the American Society of Nephrology : JASN

34768. Drug-testing in patients with pulmonary hypertension of unknown cause. (PubMed)

Drug-testing in patients with pulmonary hypertension of unknown cause. The acute haemodynamic effects of seven different drugs were serially evaluated in eight patients suffering from pulmonary hypertension of unknown cause. The following drugs were tested in randomized order: nifedipine, amrinone, isoproterenol, captopril, prostacyclin, dihydralazine and nitroglycerin. Only a reduction in pulmonary vascular resistance (PVR) of more than 30% of baseline was considered a satisfactory response

1992 European heart journal

34769. Medical therapy, symptoms, and the distress the cause: relation to quality of life in patients with angina pectoris and/or hypertension. (PubMed)

Medical therapy, symptoms, and the distress the cause: relation to quality of life in patients with angina pectoris and/or hypertension. Adverse events during drug therapy can be assessed through measurement of 2 features: their frequency and their severity. Their severity, in turn, can be measured by assessing the distress that they cause. Our goal was to relate the magnitude of the distress induced by treatment with calcium-channel blocking agents to the change in quality of life assessed (...) through psychosocial instruments in patients treated with calcium-channel blocking agents, either for hypertension or for angina pectoris.Four hundred seventy-five patients with angina pectoris were randomized to double-blind treatment with PPR (physiological pattern release) verapamil hydrochloride, amlodipine besylate, amlodipineatenolol combination, or placebo. In addition, 557 hypertensive patients were randomized either to PPR verapamil or nifedipine GITS (gastrointestinal system). Both studies

2000 Archives of internal medicine

34770. Benazepril causes in hypertension a greater reduction in left ventricular mass than does nitrendipine: a randomized study using magnetic resonance imaging. (PubMed)

Benazepril causes in hypertension a greater reduction in left ventricular mass than does nitrendipine: a randomized study using magnetic resonance imaging. To assess the comparative effects of benazepril and nitrendipine monotherapies on left ventricular mass index (LVMI) in hypertensive patients with echocardiographically determined left ventricular hypertrophy, patients with diastolic blood pressure (BP) > or = 100 mm Hg were randomized to benazepril, 10 mg, or nitrendipine, 20 mg, both given (...) a similar antihypertensive effect, benazepril led to a greater reduction in MRI-measured LVMI than did nitrendipine (-16.2% vs. -7.2%) in hypertensive patients with left ventricular hypertrophy.

1998 Journal of cardiovascular pharmacology

34771. Adenosine causes the release of active renin and angiotensin II in the coronary circulation of patients with essential hypertension. (PubMed)

Adenosine causes the release of active renin and angiotensin II in the coronary circulation of patients with essential hypertension. The aim of the study was to evaluate whether adenosine infusion can induce production of active renin and angiotensin II in human coronary circulation.Adenosine can activate angiotensin production in the forearm vessels of essential hypertensive patients.In six normotensive subjects and 12 essential hypertensive patients adenosine was infused into the left (...) anterior descending coronary artery (1, 10, 100 and 1,000 microg/min x 5 min each) while active renin (radioimmunometric assay) and angiotensin II (radioimmunoassay after high performance liquid chromatography purification) were measured in venous (great cardiac vein) and coronary arterial blood samples. In five out of 12 hypertensive patients adenosine infusion and plasma samples were repeated during intracoronary angiotensin-converting enzyme inhibitor benazeprilat (25 microg/min) administration

1999 Journal of the American College of Cardiology

34772. Co-dergocrine mesylate inhibits the increase in plasma catecholamines caused by nifedipine in essential hypertension. (PubMed)

Co-dergocrine mesylate inhibits the increase in plasma catecholamines caused by nifedipine in essential hypertension. Co-dergocrine mesylate (Cod), which inhibits norepinephrine secretion by stimulating presynaptic dopamine receptors, and has no known metabolic side effect, has an additive antihypertensive effect to that of Nifedipine (Nif). Plasma norepinephrine, epinephrine, renin activity and aldosterone have been measured after acute administration of Nif and Cod alone and in combination (...) after the second treatment. Blood pressure was significantly lower (P less than 0.05) where Cod preceded Nif. Cod caused a significant decrease in plasma norepinephrine from 293 to 202 pg.ml-1 and in epinephrine from 67 to 55 pg.ml-1. The Nif-induced increase in norepinephrine from a pre-treatment value of 293 pg.ml-1 with preceding Cod to 331 pg.ml-1 was much less than the increase with placebo as premedication, from 284 to 440 pg.ml-1. Nif caused an increase in renin activity but no increase

1990 European journal of clinical pharmacology

34773. In patients with mild hypertension, does exercise and a gradual rather than abrupt increase in fatty acid and salt intake cause less rise in cardiovascular risk factors? (PubMed)

In patients with mild hypertension, does exercise and a gradual rather than abrupt increase in fatty acid and salt intake cause less rise in cardiovascular risk factors? In a randomised, single blind controlled trial, 58 patients with mild essential hypertension were administered either a normal diet with a gradual increase in salt and fatty acid consumption (Group A, 30 cases), or an abrupt increase (Group B, 28 cases) for a period of 24 weeks. Group A patients also did more physical activity

1992 Clinical nutrition (Edinburgh, Scotland)

34774. A double dose of phenylpropanolamine causes transient hypertension. (PubMed)

A double dose of phenylpropanolamine causes transient hypertension. Phenylpropanolamine is widely used and freely available without a doctor's prescription in drug and grocery stores; it is the active ingredient in most diet aids and many cold preparations. Several cases of multiple cerebral hemorrhages associated with transient hypertension have recently been attributed to phenylpropanolamine in dosages equal to or less than that contained in two diet aids (i.e., 150 mg). Some evidence also (...) placebo. Blood pressure and heart rate were monitored throughout the study.Although 75 mg of phenylpropanolamine did not cause clinically relevant hypertension in our subjects, 150 mg of phenylpropanolamine and 75 mg of phenylpropanolamine plus 400 mg caffeine did result in significant blood pressure increases into the hypertensive range.We believe that consumers often assume that double the recommended dosage of an OTC drug is safe and more effective. We suggest that requiring a physician's

1988 The American journal of medicine

34775. Correcting for the bias caused by drop-outs in hypertension trials. (PubMed)

Correcting for the bias caused by drop-outs in hypertension trials. A major source of bias in hypertension trials can arise from patients who are withdrawn during the course of the trial because of inadequate blood pressure control. We develop a mechanism which allows for such withdrawals while preserving the potential to make an unbiased comparison of the treatment effects. The approach is illustrated using data from a large multicentre trial of two anti-hypertensive agents in patients (...) with mild to moderate essential hypertension.

1988 Statistics in medicine

34776. Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells. (PubMed)

Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells. Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced (...) hypertension [systolic blood pressure (SBP) = 156 +/- 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg. kg(-1). day(-1)) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect

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2002 American Journal of Physiology. Renal physiology

34777. Role of p47(phox) in vascular oxidative stress and hypertension caused by angiotensin II. (PubMed)

Role of p47(phox) in vascular oxidative stress and hypertension caused by angiotensin II. Hypertension caused by angiotensin II is dependent on vascular superoxide (O2*-) production. The nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase is a major source of vascular O2*- and is activated by angiotensin II in vitro. However, its role in angiotensin II-induced hypertension in vivo is less clear. In the present studies, we used mice deficient in p47(phox), a cytosolic subunit (...) of the NADPH oxidase, to study the role of this enzyme system in vivo. In vivo, angiotensin II infusion (0.7 mg/kg per day for 7 days) increased systolic blood pressure from 105+/-2 to 151+/-6 mm Hg and increased vascular O2*- formation 2- to 3-fold in wild-type (WT) mice. In contrast, in p47(phox-/-) mice the hypertensive response to angiotensin II infusion (122+/-4 mm Hg; P<0.05) was markedly blunted, and there was no increase of vascular O2*- production. In situ staining for O2*- using dihydroethidium

2002 Hypertension

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