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

The clinical records of adult patients with a diagnosis of hemolytic uremic syndrome were retrospectively reviewed with the aim of evaluating the long-term outcome of renal function. The setting is the Italian Registry of Haemolytic Uraemic Syndrome, with which 13 Nephrology Centers have participated. Clinical and laboratory data of 43 patients with hemolytic uremic syndrome were evaluated. The mean age at onset was 34.3 +/- 18.3 yr. Men and women were equally affected. No seasonal trend in presentation was observed. In 20 patients, hemolytic uremic syndrome was primitive, whereas in 23, it was associated with another disease (cancer, preeclampsia, malignant hypertension, vasculitides). Gastrointestinal symptoms were the most frequently observed prodromes. Thirty (70%) patients required dialysis during the acute phase of the disease. Six patients died during the acute phase of the disease, and one died later after discharge (overall mortality, 16%). After 1 yr of follow-up, 11 (26%) patients had recovered a normal renal function, 14 (33%) had hypertension and/or renal insufficiency, and 11 (26%) were on regular dialysis. When prognostic factors of survival and recovery of renal function were considered, it was found that older age was associated with higher mortality in the acute phase, whereas severe renal involvement at the onset of the disease (as expressed by elevated serum creatinine) was associated with a long-term unfavorable prognosis.
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PMID:Renal function at hospital admission as a prognostic factor in adult hemolytic uremic syndrome. The Italian Registry of Haemolytic Uremic Syndrome. 161 Sep 85

The role of ions and cell membrane function in the pathogenesis of benign and malignant hypertension was investigated in spontaneously hypertensive rats (SHR). Ten-week-old male SHR (n = 50) and SHR treated with deoxycorticosterone acetate (DOCA; n = 70) and 1% NaCl drinking water were studied weekly for 14 weeks. Malignant hypertension developed only in DOCA-salt SHR and was characterised by severe hypertension, failure to thrive and renal fibrinoid necrosis. Fourteen DOCA-salt SHR and one SHR died. Extracellular (serum) and intracellular (erythrocyte and muscle) Na+, K+, Mg2+, Ca2+ and muscle membrane Na+,K(+)-adenosine triphosphatase (ATPase), Ca(2+)-ATPase and Mg(2+)-ATPase were measured at various stages in the development of malignant hypertension. Three developmental phases were defined: benign, premalignant and malignant. DOCA-salt SHR showed persistent hypokalaemia. In the benign phase, there were no differences in Na+, Mg2+ and Ca2+ between SHR and DOCA-salt SHR. In the premalignant phase, serum and erythrocyte Mg2+ and ATPase activity were significantly lower in DOCA-salt SHR compared with SHR. During the late premalignant and malignant phases, intracellular Ca2+ and Na+ were significantly higher in the DOCA-salt SHR compared with SHR. In view of these findings, the abnormalities in DOCA-salt SHR during the early phases of blood pressure elevation could be contributory factors to the development of malignant hypertension.
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PMID:Altered cations and muscle membrane ATPase activity in deoxycorticosterone acetate-salt spontaneously hypertensive rats. 165 84

Malignant stroke-prone spontaneously hypertensive rats (M-SHRSP) are a useful animal model for studying juvenile malignant hypertension. Using M-SHRSP males, the effects of SQ 29,852 [(S)-1-[6-amino-2-[[hydroxy (4-phenylbutyl) phosphinyl]oxy]-1-oxohexyl]-L-proline; 30-40 mg/kg per day], captopril (30-40 mg/kg per day), hydralazine hydrochloride (10-15 mg/kg per day) and a 33% fish meal diet on the prevention and therapy of malignant hypertension were examined. Drugs and diet were given separately, beginning at weaning, maturity or adulthood. Observed effects included antihypertension, prolonged life span and prevention and/or reversal of angionecrosis. Each treatment resulted in an antihypertensive effect, but some adult rats seemed treatment-resistant. SQ 29,852 was the most effective treatment for reducing blood pressure. The life span of animals in the treated groups was extended significantly beyond that of the controls. In particular, those rats treated with either captopril or SQ 29,852 lived in excess of 500 days. This included not only those in which treatment resulted in a lowering of blood pressure, but also those whose severe hypertension was not so reduced. Angionecrosis was observed in the organs of many of the non-treated animals, including the brain, heart, kidneys and testes. Both hydralazine and the fish meal diet had a limited effect, if any, on the prevention or reversal of angionecrosis. In contrast, almost none of the rats given either captopril or SQ 29,852 showed cerebrovascular lesions or angionecrosis of the brain, heart and kidneys; angionecrosis in adult M-SHRSP kidneys disappeared within 10 or 18 days after the initiation of SQ 29,852 or captopril, respectively. This data seems to support a possible role for these two drugs not only in prevention, but also in repair, of angionecrosis independent of markedly high blood pressure in M-SHRSP. Based on our overall observations, SQ 29,852 was seen as the most effective of the treatments studied.
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PMID:Chronic treatment with captopril, SQ29,852, hydralazine and a 33% fish meal diet in malignant stroke-prone spontaneously hypertensive rats. 166 66

The three approaches (physiopathological, epidemiological and pharmacological) to the management of hypertension should converge to provide a personalized prescription of the most appropriate treatment to prevent and/or cure the cardiovascular complications of hypertension: hypertensive left ventricular hypertrophy and the risks directly related to it (haemodynamic, arrhythmic, ischaemic) may be corrected by certain antihypertensive agents (methyldopa, ACE inhibitors, some calcium antagonists) although there is no proof as yet of the benefits of this intervention (which could suppress the adaptation to the increased wall stress of the left ventricle); malignant hypertension and its cardiovascular complications have almost disappeared with modern antihypertensive therapy. Cardiac failure can be effectively prevented and cured when exclusively related to hypertension. When diastolic pressures are lowered by 8-10 mmHg cerebrovascular risk is reduced by a half and coronary risk by a quarter. Cardiovascular mortality related to hypertension is thus reduced by 20% and total mortality is thereby significantly decreased; the large scale clinical trials which provided these data were performed in the years 1965-1985 with diuretic therapy relayed by (or compared with) betablockers from 1980 onwards. These two families remain the drugs of reference in the prevention and treatment of the cardiovascular complications of hypertension. Personalized description of antihypertensive therapy should take into account the degree of risk and previous cardiovascular complications of the hypertensive patient: betablockers eventually associated with calcium antagonists are to be preferred in cases of hypertension with coronary artery disease and/or arrhythmias, severe hypertension and hypertension complicated by cardiac failure are good indications for ACE inhibitors without prejudicing other therapeutic options necessary in certain contexts, in particular aspirin therapy in patients with previous transient ischemic cerebral attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of hypertension and cardiovascular complications]. 168 21

Antihypertensive therapy reduces cardiovascular risk in patients with malignant hypertension, but has not yet been shown to reduce risk in patients with mild to moderate hypertension. The lack of significant coronary prevention in the latter group, in large-scale trials, may have resulted from methodologic problems, statistical limitations, the adverse effects of antihypertensive medications, or failure to recognize the prognostic importance of concomitant regression of left ventricular hypertrophy. To date, primary prevention studies have focused on the use of beta-blockers and diuretics, both of which may have adverse metabolic effects and neither of which is capable of modifying left ventricular hypertrophy. Future research should be directed toward evaluating coronary prevention in patients with nonmalignant hypertension who have been treated with newer agents, such as calcium channel blockers and angiotensin-converting enzyme inhibitors, each of which has been shown to regress left ventricular hypertrophy and not to have adverse metabolic effects.
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PMID:Antihypertensive therapy and coronary prevention. 170 11

Hypertension is a major disease in the black population of sub-Saharan Africa and the U.S. The prevalence of hypertension varies from 1-30% of the adult population. Differences in blood pressure (BP) between black and white patients have been documented. In this review, genetic, endocrine, and environmental characteristics, renal physiology, and cardiac function are reviewed. Racial differences in renal physiology and socioeconomic status seem to account for BP differences. Black hypertensive patients in sub-Saharan Africa are prone to cerebral hemorrhage, malignant hypertension leading to uremia, and congestive heart failure, whereas coronary artery disease is uncommon. Responses to hypotensive agents like beta-blockers and angiotensin-converting enzyme inhibitors are poor unless these agents are combined with a thiazide diuretic. Black hypertensive patients respond best to diuretics, vasodilators, or calcium channel blockers. A profiled approach to the treatment of hypertension is suggested.
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PMID:Perspectives of hypertension in black patients: black vs. white differences. 170 30

Regression of cardiovascular structural changes is a main goal of antihypertensive treatment. Nitrendipine is a calcium antagonist of the dihydropiridine group that may be given once daily. In different animal models of experimental hypertension, nitrendipine was shown to reduce blood pressure (BP) and left ventricular (LV) mass, to prevent early mortality, and to limit the development of vascular lesions. It has also been proposed that nitrendipine is able to preserve tissue integrity and increase life span in malignant hypertension, because it prevents a deleterious calcium overload in the heart and arterial vessels. In humans, the effect of nitrendipine on LV mass has been evaluated in a limited number of studies with conflicting results. It has been shown that nitrendipine is able to increase the compliance of large arteries; its effect on vascular structural changes has never been reported. In this study, nitrendipine (20 mg o.d.) was given to 10 hypertensive patients. BP, (ambulatory BP monitoring) heart rate (HR), LV mass and function (TM echo, 2D guided), forearm minimal vascular resistance (min VR = BP/max blood flow--venous occlusion plethysmography--taken as an index of vascular STC), plasma renin activity (PRA), plasma catecholamines (NE and E), and aldosterone (ALD) were measured during placebo, after 2 and 6 months of treatment. BP was significantly reduced and HR was slightly increased. After 6 months of treatment a significant reduction of LV mass index (p less than 0.001) and of min VR (p less than 0.002) was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regression of cardiovascular structural changes after long-term antihypertensive treatment with the calcium antagonist nitrendipine. 172 98

The aim of this study was to characterize the antihypertensive and vasoprotective properties of lacidipine in salt-loaded Dahl-S rats, a suitable animal model of malignant hypertension. After 9 weeks of a high (8%) sodium chloride (NaCl) diet, 80% of the untreated Dahl-S rats died (20% survival rate) whereas a 100% survival rate was observed with chronic treatment with lacidipine at doses of 0.1 (equivalent to the recommended dose in humans), 0.3, 1, and 10 mg/kg once daily by gastric gavage. The most interesting results included the following: (a) Only the highest dose tested (10 mg/kg once daily) was able to control the increase in blood pressure, which was measured 24 h after the preceding administration of drug, yet a 100% survival rate was maintained. (b) There appeared to be prevention of brain lesions, which is very likely the cause of the survival of all of the lacidipine-treated rats in this study. (c) A clear dose-related vascular protection was observed in other tissues. In conclusion, lacidipine protects against the vascular damage and concomitant increase in mortality of salt-loaded Dahl-S rats even at doses that do not adequately control the development of hypertension.
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PMID:Vascular protection of lacidipine in salt-loaded Dahl-S rats at nonsustained antihypertensive doses. 172 12

Malignant hypertension is a unique and natural model for the study of abnormalities of left ventricular function due to arterial hypertension, because the development and regression of these abnormalities can be observed in a short period. Studies of ventricular function by radionuclide ventriculography, either before or after therapy, have not been previously reported in malignant hypertensive patients. We used this methodology to study left ventricular function in 17 malignant/accelerated hypertensive patients at the time of admission to the hospital and 3, 6, and 9 months after discharge. Seventy percent of patients (12 of 17) had symptoms of congestive heart failure at admission. We compared these data with those obtained in 12 normotensive subjects and 13 mild-to-moderate untreated hypertensive patients. Blood pressure of malignant hypertensive patients was 213 +/- 26/140 +/- 17 mm Hg at admission and 165 +/- 23/101 +/- 15 after 9 months of therapy. Radionuclide ventriculography at admission showed that peak filling rates of malignant hypertensive patients (2.13 +/- 0.21 end-diastolic volume [counts] [EDV]/sec) were significantly lower than those in normotensive subjects (2.40 +/- 0.41) and in mild-to-moderate hypertensive patients (2.46 +/- 0.21). In contrast, peak ejection rates were significantly higher in malignant hypertensive patients (3.44 +/- 0.38 EDV/sec) than in the two control groups (3.01 +/- 0.32 and 3.10 +/- 0.43, respectively). Ejection fractions were similar in the three groups of patients. After 9 months of therapy, peak filling rates of malignant hypertensive patients increased to 2.38 +/- 0.35 EDV/sec, whereas peak ejection rates decreased to 2.89 +/- 0.43 EDV/sec, both not significantly different from data in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Feb
PMID:Ventricular function by radionuclide ventriculography in malignant hypertension. 173 81

Consecutive hypertensives admitted with cardiovascular complications were studied. One hundred and eight complicated hypertensives (10%) out of 1,066 medical admissions were seen in the three month study. Thirty three per cent had cerebrovascular disease, 30% ischaemic heart disease, 2% had malignant hypertension and 85% had hypertensive heart disease. All patients had uncontrolled hypertension at admission (mean blood pressure 184/115 mmHg). Twenty-four patients (22%) were newly diagnosed; of the rest of previously diagnosed hypertensives (78%), 3% had never been on treatment and 56% had dropped out of treatment, which explained their ineffective blood pressure control. However, 18% of patients had apparently been on regular follow up and treatment, and yet their blood pressure control was poor. Many patients had evidence of renal disease. The prevalence of cardiovascular risk factors was also high; 56% had hypercholesterolaemia; 46% had hypertriglyceridaemia; 44% smoked, 38% were overweight or obese, and 18% were diabetic. This indicates that hypertension is best regarded as an ingredient of a cardiovascular risk profile and its management requires multifactorial correction of all risk factors identified.
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PMID:The Mentakab Hypertension Study project. Part I--Complicated hypertensives in hospital: who are they? 177 3


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