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Hypertension Causes

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34681. Local confidential inquiry into avoidable factors in deaths from stroke and hypertensive disease. (PubMed)

, or hypertension related causes during November 1990 to October 1991.Presence of important avoidable factors and departures from minimum standards of good practice.Adequate information was obtained for 88% (123/139) of eligible cases. Agreement between the assessors was mostly satisfactory. 29% (36/123, 95% confidence interval 21% to 37%) of all cases and 44% (36/81, 34% to 55%) of those with definite hypertension had avoidable factors that may have contributed to death. These were most commonly failures (...) Local confidential inquiry into avoidable factors in deaths from stroke and hypertensive disease. To audit avoidable deaths from stroke and hypertensive disease.Details of care before death were obtained from general practitioners and other doctors, anonymised, and assessed by two experts against agreed minimum standards of good practice for detecting and managing hypertension.Health authority with population of 250,000.All patients under 75 years who died of stroke, hypertensive disease

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1993 BMJ : British Medical Journal

34682. Hypertensive response to raised intracranial pressure in infancy. (PubMed)

Hypertensive response to raised intracranial pressure in infancy. Mean arterial pressure and intracranial pressure were measured serially in six infants with intracranial hypertension (intracranial pressure greater than 20 mm Hg), and cerebral perfusion pressure was calculated from their difference. Overall, mean arterial pressure increased with rising intracranial pressure at a mean rate of 0.20 mm Hg/mm Hg. This caused a fall in cerebral perfusion pressure with increasing intracranial

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1988 Archives of Disease in Childhood

34683. Responsiveness of superficial hand veins to phenylephrine in essential hypertension. Alpha adrenergic blockade during prazosin therapy. (PubMed)

Responsiveness of superficial hand veins to phenylephrine in essential hypertension. Alpha adrenergic blockade during prazosin therapy. Patients with essential hypertension show an increase in vascular resistance. It is unclear whether this is caused by structural changes in the arterial wall or by hyperresponsiveness of vascular smooth muscle to endogenous alpha adrenergic agonists. Using the dorsal hand vein compliance technique we compared the changes in diameter of superficial veins (...) are due to structural and geometric changes in the arterial wall rather than to an increased responsiveness of postsynaptic alpha adrenergic receptors. The phenylephrine studies were repeated in seven hypertensive patients during treatment with prazosin, an alpha 1 adrenergic antagonist. The mean dose ratio of the shift in phenylephrine ED50 (ED50 during prazosin therapy/ED50 before prazosin therapy) was 6.1. This indicates that small doses of prazosin (1-2 mg) cause significant in vivo shifts

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1989 Journal of Clinical Investigation

34684. Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension. (PubMed)

, in normotensive rabbits, infusion of PGI2 reproduced the splanchnic hyperemia and caused a very small but significant increase in portosystemic shunting. These findings support the previously proposed concept that splanchnic hyperemia may contribute to the maintenance of chronic portal hypertension. Furthermore, they suggest that this effect may be partially mediated by splanchnic PGI2 production. (...) Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension. To determine the possible role of prostacyclin (PGI2) as a mediator of the splanchnic hyperemia seen with portal hypertension, the portal and mesenteric hemodynamics in normal and portal hypertensive rabbits were studied before and after cyclo-oxygenase blockade. Three weeks after partial portal vein ligation, splenic pulp pressure was elevated from 4.3 +/- 0.9 to 9.8 +/- 0.8 mmHg (p less than 0.01

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1989 Annals of Surgery

34685. Prediction of favourable responses to long term vasodilator treatment of pulmonary hypertension by short term administration of epoprostenol (prostacyclin) or nifedipine. (PubMed)

Prediction of favourable responses to long term vasodilator treatment of pulmonary hypertension by short term administration of epoprostenol (prostacyclin) or nifedipine. Eighteen patients with moderate to severe pulmonary hypertension were studied, nine with intracardiac shunts and nine without. The effects of an incremental infusion of epoprostenol (prostacyclin) (0.5-8 ng/kg per minute) or sublingual nifedipine (20-30 mg) were compared with the response to three months' treatment with oral (...) nifedipine. Both epoprostenol and sublingual nifedipine caused a fall in pulmonary vascular resistance and pressure and a rise in cardiac output. Patients with intracardiac shunts had higher systemic blood flows than those without shunts. Exercise in the shunt group was accompanied by systemic desaturation and hyperventilation. Analysis of individual results showed that the size of the response was inversely related to the severity of the pulmonary vascular disease. A good long term response

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1988 British Heart Journal

34686. Segmental portal hypertension. (PubMed)

Segmental portal hypertension. Isolated obstruction of the splenic vein leads to segmental portal hypertension, which is a rare form of extrahepatic portal hypertension, but it is important to diagnose, since it can be cured by splenectomy. In a review of the English literature, 209 patients with isolated splenic vein obstruction were found. Pancreatitis caused 65% of the cases and pancreatic neoplasms 18%, whereas the rest was caused by various other diseases. Seventy-two per cent (...) of the patients bled from gastroesophageal varices, and most often the bleeding came from isolated gastric varices. The spleen was enlarged in 71% of the patients. A correct diagnosis in connection with the first episode of bleeding was made in only 49%; 22% were operated on because of gastrointestinal bleeding, but the cause of bleeding was not found. The diagnosis should be suspected in patients with gastroesophageal varices, but without signs of a liver disease, especially if isolated gastric varices

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1986 Annals of Surgery

34687. Chronic caffeine administration exacerbates renovascular, but not genetic, hypertension in rats. (PubMed)

or normal drinking water, and systolic blood pressure was monitored for 6 wk. Caffeine markedly exacerbated the severity of hypertension in 2K-1C rats and caused histological changes consistent with malignant hypertension. 6 wk after surgery, systolic blood pressure, plasma renin activity, and creatinine clearance in control 2K-1C rats were 169 +/- 5 mmHg (mean +/- SEM), 4.4 +/- 0.5 ng AI X ml-1 X h-1, and 2.9 +/- 0.2 ml/min, respectively; as compared with 219 +/- 4 mmHg, 31.8 +/- 7.8 ng AI X ml-1 X h-1 (...) Chronic caffeine administration exacerbates renovascular, but not genetic, hypertension in rats. The purpose of this study was to determine whether or not caffeine would exacerbate renovascular hypertension. Therefore, we examined the effects of chronic caffeine administration on arterial blood pressure in rats subjected to either unilateral renal artery clipping (2K-1C rats) or sham-operation. Animals in each group were randomly assigned to receive either 0.1% caffeine in their drinking water

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1986 Journal of Clinical Investigation

34688. Neurogenic hypertension associated with an excessively high excretion rate of catecholamine metabolites. (PubMed)

Neurogenic hypertension associated with an excessively high excretion rate of catecholamine metabolites. A 60 year old hypertensive patient suffered several cerebral infarctions. A phaeochromocytoma was suspected because the excretion rates of vanillylmandelic acid and its methoxy derivatives were raised and the patient had hypertensive crises. No tumour was found, however, by 131mI-iodobenzylguanidine scintigraphy and computed tomography of the abdomen. Moreover, the enhanced orthostatic (...) plasma catecholamine response suggested that the high excretion rates of catecholamine metabolites were more likely to be caused by the syndrome of raised catecholamines after cerebrovascular accidents than a phaeochromocytoma. A phaeochromocytoma should not be diagnosed within several months of cerebral infarction without first excluding the possibility of a hyperadrenergic state induced by cerebral infarction.

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1987 British Heart Journal

34689. Role of liver atrophy, hepatic resection and hepatocyte hyperplasia in the development of portal hypertension in biliary disease. (PubMed)

is equally important. If so, we hypothesised that patients with biliary obstruction and a coincident condition such as liver atrophy, or hepatic resection, with the potential of accelerating the hepatocyte proliferation caused by biliary obstruction itself, might be expected to develop portal hypertension earlier than patients with biliary obstruction alone. To examine this concept we studied 10 patients with postcholecystectomy bile duct stricture, portal hypertension and liver atrophy, or hepatic (...) Role of liver atrophy, hepatic resection and hepatocyte hyperplasia in the development of portal hypertension in biliary disease. Portal fibrosis is considered to be pivotal in the pathogenesis of portal hypertension associated with extrahepatic biliary obstruction. The histological features, however, include diffuse hepatocyte hyperplasia as well as portal fibrosis, but not cirrhosis, and it is possible that the contribution of hepatocyte hyperplasia in the initiation of portal hypertension

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1987 Gut

34690. Perfusion Lung Scans Provide a Guide to Which Patients With Apparent Primary Pulmonary Hypertension Merit Angiography (PubMed)

pulmonary hypertension, whereas all 46 patients with thromboembolic hypertension had one or more defects that were segmental in size or larger. These data indicate that a perfusion lung scan should be done in patients with pulmonary hypertension of uncertain cause and that those with one or more segmental or larger defects merit pulmonary angiography before being diagnosed as having primary pulmonary hypertension. (...) Perfusion Lung Scans Provide a Guide to Which Patients With Apparent Primary Pulmonary Hypertension Merit Angiography There is hesitancy, based on the perceived risk, to do pulmonary angiography in patients believed to have primary pulmonary hypertension. Yet pulmonary hypertension due to major-vessel, chronic thromboembolism mimics primary pulmonary hypertension clinically and on standard laboratory tests. Because thromboembolic pulmonary hypertension is potentially remediable

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1988 Western Journal of Medicine

34691. Growth factor expression in aorta of normotensive and hypertensive rats. (PubMed)

Growth factor expression in aorta of normotensive and hypertensive rats. Hypertension causes biochemical and morphological changes in the vessel wall by unknown mechanisms. Locally produced substances may have a role in mediating these vascular changes. We have studied the expression of platelet-derived growth factor (PDGF) B chain and PDGF A chain, insulin-like growth factor (IGF)-I and IGF-II, endothelial cell growth factor (ECGF), basic fibroblast growth factor (bFGF), and transforming (...) growth factor-beta (TGF-beta) in aortic tissue from normotensive rats and rats made hypertensive by deoxycorticosterone (DOC)/salt treatment. Using Northern blotting, we found that genes for each of these growth factors were transcriptionally active in the aorta of both normotensive and hypertensive rats. TGF-beta aortic mRNA levels increased up to threefold as a result of DOC/salt hypertension. In contrast, no major changes in the expression of either PDGF chain, IGF-I or II, ECGF, or bFGF were

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1989 Journal of Clinical Investigation

34692. The surgeon's role in the management of portal hypertension. (PubMed)

The surgeon's role in the management of portal hypertension. Patients with portal hypertension are referred to surgeons for several reasons. These include the management of continued active variceal bleeding; therapy after a variceal bleed to prevent further recurrent bleeds; consideration for prophylactic surgical therapy to prevent the first variceal bleed; or, rarely, an unusual cause of portal hypertension which may require some specific surgical therapy. Injection sclerotherapy is the most (...) bleeding as well as for long-term management, particularly in alcoholic cirrhotic patients. For acute variceal bleeding the surgical alternative to sclerotherapy or shunting is simple staple-gun esophageal transection, whereas in long-term management the main alternative is an extensive devascularization and transection operation. Liver transplantation is the only therapy that cures both the portal hypertension and the underlying liver disease. All patients with cirrhosis and portal hypertension should

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1989 Annals of Surgery

34693. Failure of postnatal adaptation of the pulmonary circulation after chronic intrauterine pulmonary hypertension in fetal lambs. (PubMed)

). Pulmonary hypertension for greater than 8 d increased the wall thickness of small pulmonary arteries (P less than 0.001). Compared with controls, hypertensive animals had higher pulmonary artery pressure, lower pulmonary blood flow, and predominant right-to-left ductus shunting after cesarean-section delivery (P less than 0.0001). We conclude that chronic pulmonary hypertension in utero, in the absence of hypoxemia or sustained increases in blood flow, causes abnormal fetal pulmonary vasoreactivity (...) Failure of postnatal adaptation of the pulmonary circulation after chronic intrauterine pulmonary hypertension in fetal lambs. To determine the effects of chronic intrauterine pulmonary hypertension on the perinatal pulmonary circulation, we induced chronic elevations of pulmonary artery pressure in 24 late-gestation fetal lambs by maintaining partial compression of the ductus arteriosus with an inflatable vascular occluder. Pulmonary artery pressure was increased from 44 +/- 1 to 62 +/- 3 mmHg

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1989 Journal of Clinical Investigation

34694. Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. (PubMed)

to approximately 5-500 ng/ml), caused a dose- and time-dependent release of potassium, thromboxane A2, and prostaglandin I2, but not of lactate dehydrogenase, into the recirculating medium, as well as a dose-dependent liberation of the prostanoids into the bronchoalveolar space. These events were paralleled by a dose-dependent pulmonary hypertension, and studies with different inhibitors collectively indicated that the vasoconstrictor response was mediated predominantly by pulmonary thromboxane generation (...) Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. Escherichia coli hemolysin has been implicated as a pathogenicity factor in extraintestinal E. coli infections including sepsis. In the present study the effects of intravascular administration of hemolysin were investigated in isolated blood-free perfused rabbit lungs. Low concentrations of the toxin in the perfusate (0.05-5 hemolytic units/ml, corresponding

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1989 Journal of Clinical Investigation

34695. Medical conditions underlying retinal vein occlusion in patients with glaucoma or ocular hypertension. (PubMed)

, and these prevalence rates were strikingly similar to the rates in patients with recurrence but without glaucoma. The data suggest that glaucoma or ocular hypertension has a less prominent aetiological role in the development of a retinal vein occlusion than underlying medical causes and that full medical assessment is worthwhile. (...) Medical conditions underlying retinal vein occlusion in patients with glaucoma or ocular hypertension. Forty-three patients with glaucoma and 24 patients with ocular hypertension presenting with a retinal vein occlusion were medically assessed. The prevalence of systemic hypertension was 60.5% in those with glaucoma and 66.6% with ocular hypertension. The prevalence of hyperlipidaemia was 38.1% in those with glaucoma and 37.5% in those with ocular hypertension. These findings were compared

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1989 The British journal of ophthalmology

34696. Altered vascular function in fetal programming of hypertension. (PubMed)

to the NO donor sodium nitroprusside was also decreased and was associated with reduced (by 50% to 65%) cGMP levels and sGC expression. cGMP analogues caused comparable vasorelaxation in the 2 groups. Expression of K(Ca) (another important mediator of NO action) and relaxation to the K(Ca) opener NS1619 were unchanged by antenatal diet.Maternal protein deprivation, which leads to hypertension in the offspring, is associated with diminished NO-dependent relaxation of major organ (cerebral) microvasculature (...) Altered vascular function in fetal programming of hypertension. Reduced endothelium-dependent vasorelaxation partly due to loss of nitric oxide (NO) bioavailability occurs in most cases of chronic hypertension. Intrauterine nutritional deprivation has been associated with increased risk for hypertension and stroke, associated with relaxant dysfunction and decreased vascular compliance, but the underlying mechanisms are not known. The present studies were undertaken to investigate whether

2002 Stroke

34697. Effect of Domperidone on the Bromocriptine-Induced Antihypertensive Action in Hypertensive Patients. (PubMed)

Effect of Domperidone on the Bromocriptine-Induced Antihypertensive Action in Hypertensive Patients. Dopaminergic receptors have been involved in the cardiovascular and renin-angiotensin systems (RAS). We have recently reported that bromocriptine is an effective antihypertensive drug by stimulating DA(2) dopaminergic receptors. However, the nature of the dopaminergic receptors in RAS has not been established. Ten outpatients with essential hypertension were treated at the Vargas Hospital (...) with bromocriptine (BR) (11.25 mg day(minus sign1)), a DA(2) dopaminergic agonist, for a 2-week period, after which an oral dose of 30 mg day(minus sign1) of domperidone (DO), a peripheric DA(2) dopaminergic antagonist, was added for 2 additional weeks. The active period was preceeded by a 2-week placebo period. Bromocriptine decreased blood pressure (BP) significantly by 19/9 mm Hg (systolic/diastolic BP). Bromocriptine did not cause heart rate (HR) changes. Bromocriptine decreased plasma aldosterone (ALD

1995 American journal of therapeutics Controlled trial quality: uncertain

34698. Effect of Bisoprolol and Atenolol on Left Ventricular Mass in Patients with Essential Hypertension. (PubMed)

Effect of Bisoprolol and Atenolol on Left Ventricular Mass in Patients with Essential Hypertension. A new beta-blocker, bisoprolol, was compared to atenolol for antihypertensive efficacy and ability to cause regression of left ventricular mass. Twenty-eight patients were randomized into this 8-week, double-blind, dose-escalating trial. Echocardiography was performed in 18 of these patients at baseline and after 8 weeks of therapy to determine left ventricular (LV) mass indices. Both drugs (...) caused a reduction in blood pressure, although bisoprolol caused a significantly greater reduction than did atenolol in diastolic pressure (p < 0.05) and a trend toward a greater reduction in systolic pressure (p < 0.096) as measured by cuff. Comparisons showed a significantly greater reduction in mean LV mass indices with bisoprolol than with atenolol (p < 0.05). A new beta-blocker, bisoprolol, was compared to atenolol for antihypertensive efficacy and ability to cause regression of left ventricular

1994 American journal of therapeutics Controlled trial quality: uncertain

34699. Enalapril and Lisinopril in Renovascular Hypertension Antihypertensne and Hormonal Effects of Two New Angio-Tensin-Converting-Enzyme (ACE) Inhibitors. (PubMed)

Enalapril and Lisinopril in Renovascular Hypertension Antihypertensne and Hormonal Effects of Two New Angio-Tensin-Converting-Enzyme (ACE) Inhibitors. We assessed the antihypertensive and hormonal effects of two new angiotensin converting enzyme (ACE) inhibitors. enalapril (MK-421) and lisinopril (MK-521) in 22 patients with renovascular hypertension. All patients had angiographically verified renal artery lesions, 3 had bilateral renal artery stenosis and one a stenosis in a single kidney (...) of 40 mg o.d. at 6 h: mean supine BP fall-25/28 mmHg and standing-33/31 mm Hg. Both drugs significantly inhibited serum ACE to about 5 to 10% of initial values and with a duration for more than 24 h. Both drugs also caused a decrease in plasma All levels and also in plasma aldosterone concentrations. There were no toxic effects and no serious side effects. Careful monitoring of biochemical variables showed no significant changes. We conclude that both enalapril and lisinopril are effective and very

1984 Scandinavian journal of urology and nephrology Controlled trial quality: uncertain

34700. Influence of drugs and gender on the arterial pulse wave and natriuretic peptide secretion in untreated patients with essential hypertension. (PubMed)

Influence of drugs and gender on the arterial pulse wave and natriuretic peptide secretion in untreated patients with essential hypertension. Recent studies have suggested a differential influence of mean pressure and pulse pressure on myocardial infarction and stroke, and differences among the major drugs in their efficacy at preventing these individual endpoints. We hypothesized that antihypertensive drugs have differing influences upon the pulse wave even when their effects on blood pressure (...) are the same. We studied 30 untreated hypertensive patients, aged 28-55 years, who were rotated through six 6-week periods of daily treatment with amlodipine 5 mg, doxazosin 4 mg, lisinopril 10 mg, bisoprolol 5 mg, bendrofluazide 2.5 mg or placebo. The best drug was repeated at the end of the rotation. Blood pressure readings and radial pulse tonometry (by Sphygmocor) were performed at each visit, and blood was taken for measurement of levels of atrial natriuretic peptide and brain natriuretic peptide (BNP

2002 Clinical science (London, England : 1979) Controlled trial quality: uncertain

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