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Hypertension Causes

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34661. Familial persistent pulmonary hypertension of the newborn resulting from misalignment of the pulmonary vessels (congenital alveolar capillary dysplasia). (PubMed)

Familial persistent pulmonary hypertension of the newborn resulting from misalignment of the pulmonary vessels (congenital alveolar capillary dysplasia). Misalignment of the pulmonary veins with congenital alveolar capillary dysplasia, although rare, has been reported as a cause of persistent pulmonary hypertension of the newborn. Reported cases have been mainly sporadic. Familial occurrence has been reported in only three instances. We present affected sibs with this condition. In addition

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1998 Journal of Medical Genetics

34662. 'Home hypertension': exploring the inverse white coat response. (PubMed)

'Home hypertension': exploring the inverse white coat response. The classical 'white coat response' to blood pressure measurement has been studied thoroughly. However, little is known about patients showing a reverse pattern, i.e. who have lower blood pressure readings at the clinic than outside healthcare facilities.To estimate the proportion of patients whose blood pressure levels as determined by self-measurements at home are higher than those taken at the clinic and to explore possible (...) -inflating device when still at the clinic were higher than in the rest of the sample.The results point to measurement bias being at least partly responsible for higher blood pressure readings outside the clinic. Automatic measurement devices used for self/home blood pressure measurement seem to cause an alerting reaction analogous to the well-described 'white coat response'.

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1998 The British Journal of General Practice

34663. Chronic hypertension and altered baroreflex responses in transgenic mice containing the human renin and human angiotensinogen genes. (PubMed)

Chronic hypertension and altered baroreflex responses in transgenic mice containing the human renin and human angiotensinogen genes. We have generated a transgenic model consisting of both the human renin and human angiotensinogen genes to study further the role played by the renin-angiotensin system in regulating arterial pressure. Transgenic mice containing either gene alone were normotensive, whereas mice containing both genes were chronically hypertensive. Plasma renin activity and plasma (...) angiotensin II levels were both markedly elevated in the double transgenic mice compared with either single transgenic or nontransgenic controls. The elevation in blood pressure caused by the human transgenes was independent of the genotype at the endogenous renin locus and was equal in mice homozygous for the Ren-1c allele or in mice containing one copy each of Ren-1c, Ren-1d, or Ren-2. Chronic overproduction of angiotensin II in the double transgenic mice resulted in a resetting of the baroreflex

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1996 Journal of Clinical Investigation

34664. Science, medicine, and the future. Hypertension. (PubMed)

Science, medicine, and the future. Hypertension. The abundance of drugs now available for treating hypertension, and evidence that small reductions in blood pressure reverse the associated risk of stroke have shifted clinical concerns away from hypertension. However, we do not understand the cause of hypertension in 95% of patients, fail to achieve a normal blood pressure in 50% of patients, and are unable fully to reverse the cardiac and vascular changes that predate the diagnosis (...) and treatment of hypertension. Consequently, hypertension remains the commonest cause of strokes in Britain and of renal failure in the United States. Essential hypertension is a polygenic disease whose understanding can now be advanced through molecular genetic analyses. Several different syndromes are likely to be recognised; most will be due to interactions between genetic and environmental factors, but there are also likely to be further monogenic syndromes in families with multiple affected members

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1997 BMJ : British Medical Journal

34665. Primary pulmonary hypertension and human immunodeficiency virus infection (PubMed)

and radiological evaluations revealed no underlying cause. Microscopic examination of postmortem lung tissue revealed findings consistent with grade V pulmonary hypertension. Electron microscopic analysis and polyermase chain reaction detection of HIV-DNA from dissected pulmonary arterioles failed to provide any supportive evidence to suggest productive infection of the pulmonary arteriolar endothelial cells by HIV-1. Although HIV-1 likely plays a role in the pathogenesis of primary pulmonary hypertension (...) Primary pulmonary hypertension and human immunodeficiency virus infection This report details the case of a 42-year-old homosexual Caucasian male with infection due to human immunodeficiency virus type 1 (HIV-1) who presented with a four-month history of progressive dyspnea and was found to have clinical and hemodynamic evidence of severe pulmonary hypertension. He had had no opportunistic infections, and had a T helper lymphocyte count of 200×10(6)/L. Extensive clinical laboratory

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1997 The Canadian Journal of Infectious Diseases

34666. Prolonged endothelin A receptor blockade attenuates chronic pulmonary hypertension in the ovine fetus. (PubMed)

Prolonged endothelin A receptor blockade attenuates chronic pulmonary hypertension in the ovine fetus. Based on past studies of an experimental model of severe intrauterine pulmonary hypertension, we hypothesized that endothelin-1 (ET-1) contributes to high pulmonary vascular resistance (PVR), hypertensive lung structural changes, and right ventricular hypertrophy (RVH) caused by prolonged closure of the ductus arteriosus. To test this hypothesis, we studied the effects of BQ 123, a selective (...) of experimental perinatal pulmonary hypertension.

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1997 Journal of Clinical Investigation

34667. Treatment of primary pulmonary hypertension with continuous intravenous prostacyclin. (PubMed)

Treatment of primary pulmonary hypertension with continuous intravenous prostacyclin. Our ultimate goal in treating patients is to improve their quality of life and to increase survival. The optimal treatment for primary pulmonary hypertension will continue to change as our understanding of its causes improves and as progress is made in lung transplantation. There is no one best treatment for all patients. Optimal medical and surgical treatment must be tailored to the individual with changes (...) in therapeutic regimens based on serial evaluations. Quality of life and survival have improved with current treatments and the future should offer additional therapies-inhaled nitric oxide, endothelin receptor blockers, and other modulators of the pulmonary vascular bed-to improve further the treatment of this disease. In conclusion, although primary pulmonary hypertension, if untreated, is most often a rapidly progressive and fatal disease, recent advances in the treatment have significantly improved

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1997 Heart

34668. Neck pain as a presenting symptom in malignant hypertension. (PubMed)

Neck pain as a presenting symptom in malignant hypertension. Neck pain, unrelated to trauma, is relatively common and is usually presumed to be musculoskeletal in origin. A patient presented with an unusual and serious cause of neck pain-malignant hypertension. The mechanism of the neck pain may be incipient tonsillar herniation of the cerebellum caused by raised intracranial pressure.

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1997 Journal of accident & emergency medicine

34669. Nitric oxide and prostacyclin as test agents of vasoreactivity in severe precapillary pulmonary hypertension: predictive ability and consequences on haemodynamics and gas exchange (PubMed)

Nitric oxide and prostacyclin as test agents of vasoreactivity in severe precapillary pulmonary hypertension: predictive ability and consequences on haemodynamics and gas exchange In patients with primary pulmonary hypertension who respond to vasodilators acutely, survival can be improved by the long term use of calcium channel blockers. However, testing for such a response with calcium channel blockers or prostacyclin (PGI2) may cause hypotension and adversely affect gas exchange. Nitric oxide (...) < 0.05) and increased venous admixture (28 (9) versus 14 (4)% with PGI2 and 22 (9) versus 13 (5)% with nifedipine, p < 0.05).NO inhalation can accurately predict a vasodilator response to nifedipine in patients with severe pulmonary hypertension without adverse effects on systemic haemodynamics and gas exchange. This absence of side effects may make it a more appropriate agent for testing the vasodilator response.

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1997 Thorax

34670. Early therapeutic experience with the endothelin antagonist BQ-123 in pulmonary hypertension after congenital heart surgery (PubMed)

Early therapeutic experience with the endothelin antagonist BQ-123 in pulmonary hypertension after congenital heart surgery To assess the effect of endothelin type A (ET(A)) receptor antagonism in infants with pulmonary hypertension following corrective surgery for congenital heart disease.Open label, preliminary study.Tertiary paediatric cardiothoracic surgical centre.Three infants (aged 3 weeks, 7 weeks, and 8 months) with postoperative pulmonary hypertension unresponsive to conventional (...) treatment, including inhaled nitric oxide.Patients received incremental intravenous infusions (0.1 to 0.3 mg/kg/h) of the ET(A) receptor antagonist BQ-123.The response to BQ-123 administration was determined using continuous invasive monitoring of cardiorespiratory variables.BQ-123 infusion caused a reduction in the ratio of pulmonary to systemic pressures (0.62 (0.01) to 0.52 (0.03), mean (SEM)) with an accompanying decrease in right ventricular stroke work index (4.6 (0.4) to 2.5 (0.3) g/m

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1999 Heart

34671. 1999 Canadian recommendations for the management of hypertension (PubMed)

and the personal files of the authors were used to identify other studies. All relevant articles were reviewed, classified according to study design and graded according to levels of evidence.A high value was placed on the avoidance of cardiovascular morbidity and premature death caused by untreated hypertension.Harms and costs: The diagnosis and treatment of hypertension with pharmacological therapy will reduce the blood pressure of patients with sustained hypertension. In certain settings, and for specific (...) 1999 Canadian recommendations for the management of hypertension To provide updated, evidence-based recommendations for health care professionals on the management of hypertension in adults.For patients with hypertension, there are both lifestyle options and pharmacological therapy options that may control blood pressure. For those patients who are using pharmacological therapy, a range of antihypertensive drugs is available. The choice of a specific antihypertensive drug is dependent upon

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1999 CMAJ: Canadian Medical Association Journal

34672. Negative stress echocardiographic responses in normotensive and hypertensive patients with angina pectoris, positive exercise stress testing, and normal coronary arteriograms (PubMed)

Negative stress echocardiographic responses in normotensive and hypertensive patients with angina pectoris, positive exercise stress testing, and normal coronary arteriograms To systematically compare the results of dobutamine stress echocardiography in matched groups of hypertensive and normotensive patients with anginal chest pain and normal coronary arteriograms (CPNA).University hospital.33 patients with exertional anginal chest pain, a positive exercise stress ECG, and a completely normal (...) coronary arteriogram; 17 had a history of systemic hypertension (14 women; mean (SD) age 57 (6) years), and 16 had no hypertensive history (12 women; age 54 (9) years).Ambulatory ECG monitoring, dobutamine stress echocardiography, and thallium-201 single photon emission computed tomography (SPECT) were performed in all subjects.All patients had normal left ventricular systolic function at rest and none fulfilled the criteria for ventricular hypertrophy. Eight normotensive patients and 10 hypertensive

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2000 Heart

34673. Gene transfer of the neuronal NO synthase isoform to cirrhotic rat liver ameliorates portal hypertension (PubMed)

endothelin-1-induced contractility of perisinusoidal stellate cells. Finally, in 2 different in vivo models of cirrhosis and portal hypertension, transduction of livers with recombinant Ad.nNOS significantly reduced intrahepatic resistance and portal pressure. The data highlight the feasibility of gene transfer to diseased liver and hepatic cells and demonstrate the potential of a novel therapy for portal hypertension caused by cirrhosis. (...) Gene transfer of the neuronal NO synthase isoform to cirrhotic rat liver ameliorates portal hypertension Reduced production of nitric oxide (NO) in the cirrhotic liver results from a defect in hepatic endothelial cell nitric oxide synthase (ecNOS) and appears to contribute to the high intrahepatic resistance and portal hypertension typical of cirrhosis. Therefore, we postulated that targeting a heterologous NOS isoform to sinusoidal endothelial cells or other perisinusoidal cells

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2000 Journal of Clinical Investigation

34674. Treatment with epoprostenol reverts nitric oxide non-responsiveness in patients with primary pulmonary hypertension (PubMed)

to NO in patients with primary pulmonary hypertension. Thus the addition of NO to epoprostenol treatment might cause further improvement in the course of the disease. (...) Treatment with epoprostenol reverts nitric oxide non-responsiveness in patients with primary pulmonary hypertension To assess whether long term treatment with epoprostenol might restore primary non-responsiveness to nitric oxide (NO) in patients with primary pulmonary hypertension.Seven patients with primary pulmonary hypertension receiving intravenous epoprostenol continuously because of failure of NO to influence pulmonary haemodynamics during initial testing were followed over a period of 13

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2000 Heart

34675. Racial variation in cardiovascular morbidity and mortality in essential hypertension (PubMed)

hypertension who had undergone 24 hour ambulatory intra-arterial blood pressure monitoring.Follow up for assessment of all cause morbidity and mortality over a mean (SD) of 9.2 (4.1) years.Non-cardiovascular death, coronary death, cerebrovascular death, peripheral vascular death, non-fatal myocardial infarction, non-fatal stroke, coronary revascularisation.South Asians had the highest all cause event rate of 3.46, compared with 2.50 (NS) and 0.90 (p = 0.002) events/100 patient-years for whites and Afro (...) Racial variation in cardiovascular morbidity and mortality in essential hypertension To perform a longitudinal comparison of morbidity and mortality among white, south Asian and Afro-Caribbean hypertensive patients in relation to baseline demographic characteristics and clinic and ambulatory blood pressure variables.Observational follow up study.District general hospital and community setting in Harrow, England.528 white, 106 south Asian, and 54 Afro-Caribbean subjects with essential

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2000 Heart

34676. Pathophysiological role of leptin in obesity-related hypertension (PubMed)

Pathophysiological role of leptin in obesity-related hypertension To explore the pathophysiological role of leptin in obesity-related hypertension, we examined cardiovascular phenotypes of transgenic skinny mice whose elevated plasma leptin concentrations are comparable to those seen in obese subjects. We also studied genetically obese KKA(y) mice with hyperleptinemia, in which hypothalamic melanocortin system is antagonized by ectopic expression of the agouti protein. Systolic blood pressure (...) (BP) and urinary catecholamine excretion are elevated in transgenic skinny mice relative to nontransgenic littermates. The BP elevation in transgenic skinny mice is abolished by alpha(1)-adrenergic, beta-adrenergic, or ganglionic blockers at doses that do not affect BP in nontransgenic littermates. Central administration of an alpha-melanocyte-stimulating hormone antagonist causes a marked increase in cumulative food intake but no significant changes in BP. The obese KKA(y) mice develop BP

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2000 Journal of Clinical Investigation

34677. Hypertension in mice lacking 11β-hydroxysteroid dehydrogenase type 2 (PubMed)

Hypertension in mice lacking 11β-hydroxysteroid dehydrogenase type 2 Deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. However, the disorder is usually incompletely corrected by suppression of cortisol, suggesting additional and irreversible changes, perhaps in the kidney (...) . To examine this further, we produced mice with targeted disruption of the 11beta-HSD2 gene. Homozygous mutant mice (11beta-HSD2(-/-)) appear normal at birth, but approximately 50% show motor weakness and die within 48 hours. Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone. Young adult 11beta-HSD2(-/-) mice are markedly hypertensive, with a mean arterial blood pressure of 146 +/- 2 mmHg, compared with 121

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1999 Journal of Clinical Investigation

34678. Pulmonary hypertension secondary to neurofibromatosis: intimal fibrosis versus thromboembolism (PubMed)

evidence of chronic thromboembolic pulmonary hypertension. Severe intimal fibrosis consistent with vascular involvement with neurofibromatosis was found on endarterectomy with no evidence of pulmonary thromboembolism. Neurofibromatosis of pulmonary arteries should be considered as a possible cause of pulmonary hypertension. (...) Pulmonary hypertension secondary to neurofibromatosis: intimal fibrosis versus thromboembolism Neurofibromatosis has been known to involve blood vessels throughout the body. Pulmonary involvement with interstitial fibrosing alveolitis has been described but no case of pulmonary vascular involvement has been reported to date. A 51 year old patient with cutaneous neurofibromatosis is described who presented with severe pulmonary hypertension and radiographic, scintigraphic, and angiographic

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1999 Thorax

34679. A Locus for an Autosomal Dominant Form of Progressive Renal Failure and Hypertension at Chromosome 1q21 (PubMed)

yielded a maximum LOD score of 4.71 at a recombination fraction of 0. Recombination mapping defined an interval of approximately 11.6 cM, between the markers at loci D1S2696 and D1S2635, that contains the disease gene. Localization of the disease-causing gene in this family represents a necessary step toward isolation of the defective gene and toward a deeper understanding of the mechanisms of hypertension and progressive renal failure. (...) A Locus for an Autosomal Dominant Form of Progressive Renal Failure and Hypertension at Chromosome 1q21 Linkage studies were performed in a large family with an autosomal dominant phenotype characterized by nephropathy and hypertension. In this family of Iraqi Jewish origin, the nephropathy develops into progressive renal failure. By performing a genomewide linkage search, we localized the disease gene to chromosome 1q21; the highest LOD score was obtained for the marker at locus D1S305, which

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2000 American Journal of Human Genetics

34680. BMPR2 Haploinsufficiency as the Inherited Molecular Mechanism for Primary Pulmonary Hypertension (PubMed)

BMPR2 Haploinsufficiency as the Inherited Molecular Mechanism for Primary Pulmonary Hypertension Primary pulmonary hypertension (PPH) is a potentially lethal disorder, because the elevation of the pulmonary arterial pressure may result in right-heart failure. Histologically, the disorder is characterized by proliferation of pulmonary-artery smooth muscle and endothelial cells, by intimal hyperplasia, and by in situ thrombus formation. Heterozygous mutations within the bone morphogenetic protein (...) and between families. Taken together, these studies illustrate the considerable heterogeneity of BMPR2 mutations that cause PPH, and they strongly suggest that additional factors, genetic and/or environmental, may be required for the development of the clinical phenotype.

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2000 American Journal of Human Genetics

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