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

The object of this study was to establish whether cardioselectivity of atenolol confers any advantage over noncardioselective beta-blockade in the treatment of hypertension. A dose of atenolol was established on the basis of morning mean systolic blood pressure (mean of 5 readings) in 27 long-standing hypertensive patients previously controlled on one of three nonselective beta-blockers: propranolol, oxprenolol, or pindolol. Most patients were also taking a diuretic. A crossover trial was then conducted of atenolol and the previous nonselective beta-blocker, each drug being given for 8 wk in randomized order. Other drugs were kept constant. At the end of each 8-wk period a morning test of blood pressure and pulse rate was done, an 11:30 A.M. blood sample was taken for estimation of drug concentration, and spirometry was performed. During the eighth week a glucose tolerance test, fasting lipids, and other biochemical and hematologic estimations were done. On a separate occasion a late morning study was done on the response of blood pressure and pulse rate to three kinds of stress: bicycle ergometer, mental arithmetic, and handgrip. At dosage levels of atenolol giving a mean resting systolic blood pressure equal to that during nonselective beta-blockade, diastolic levels on atenolol tended to be lower at rest and during the mental and handgrip forms of stress. Serum creatinine levels on atenolol were lower than during nonselective beta-blockade. Anti-dioxyribonucleic acid (DNA) titers remained normal in all patients. There was no difference in lung function. There was little difference in glucose and insulin levels during glucose tolerance tests in these patients, half of whom were diabetic. There were no serious side effects but there were a few surprising ones such as vivid dreams in three and muscle cramps in one patient.
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PMID:Atenolol and three nonselective beta-blockers in hypertension. 3 Dec 59

Two patients with kidney transplants had hypertensive encephalopathy and rapidly progressive kidney failure 10 weeks and 18 months postoperatively. In one patient renal failure was associated with erythrocytosis. Absence of proteinuria, despite progressive renal insufficiency in both patients, suggested that these abnormalities were not due to rejection episodes. Subsequently, angiography proved that each of these patients had renal-artery stenosis. Surgical repair of this lesion increased creatinine clearance at least threefold, and the hypertension and erythrocytosis disappeared. Apparent "rejection" episodes in which there is no proteinuria should alert clinicians to the possiblity of renal-artery stenosis of the graft. Restoration of kidney function and amelioration of hypertension may follow revascularisation, even after many months of renal ischaemia producing severe uraemia.
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PMID:Hypertensive crisis, erythrocytosis, and uraemia due to renal-artery stenosis of kidney transplants. 4 23

Captopril (SQ 14 225), an orally active inhibitor of angiotensin-converting enzyme, was given to 7 hypertensive patients with chronic renal failure whose plasma-creatinine ranged from 1.5--7.4 mg/dl; whose plasma-renin activity was normal; whose hypertension was not controlled by previous therapy consisting in 5 patients of three or more antihypertensive drugs; and whose blood-pressures averaged 176/111 +/- 11/3 mm Hg. Inhibition of converting enzyme by oral captopril, 200 mg twice daily, reduced blood-pressure to 156/100 +/- 9/5 mm Hg. 5 patients needed additional treatment by frusemide 40--250 mg/day orally. With this combined regimen the blood-pressure of all patients averaged 126/85 +/- 4/3 mm Hg after 8 +/- 2 weeks of captopril. The drug was well tolerated. These results suggest that inhibition of angiotensin-converting enzyme with or without sodium depletion is an efficient treatment for hypertension associated with chronic renal failure. It appears that although renin levels in patients with this condition may be "normal", they are inappropriate in relation to the subtle degree of sodium retention that occurs with this disorder.
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PMID:Innappropriate renin secretion unmasked by captopril (SQ 14 225) in hypertension of chronic renal failure. 8 Jun 34

In this study naturally occurring hypertension in wild rhesus monkeys has been noted with a frequency of 13 out of 428 monkeys examined. The maximum systolic/diastolic blood pressure was 242/140 mm of Hg. Clinically there was evidence of grade I retinopathy in one case only, otherwise the animals did not manifest any symptom to suggest illness. Biochemical examination revealed normal plasma angiotensin activity but the level of serum sodium was slightly elevated. The serum potassium, blood urea and serum creatinine values were within normal limits. Serum cholesterol was, however, elevated in two cases. All hypertensive animals were sacrificed by exsanguination and a complete autopsy was performed. It revealed left ventricular hypertrophy in almost all cases, patchy myocardial degeneration with fibrosis in 3 animals and advanced renal disease only in 3 cases. It therefore appears that most of these cases of hypertension belonged to the idiopathic group.
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PMID:Spontaneously occurring hypertension in wild Rhesus monkeys. 15 Nov 70

Fortynine patients of 193 admitted (25%) with second and third degree burns to 3 hospitals in different geographical areas of the United States developed a hypertensive crisis within three to four days after admission. The crisis usually lasted from 5 days to about two weeks. Serum sodium levels decreased significantly in hypertensive patients one or two days before the peak of the hypertensive crisis and, in the Center where it was measured, plasma renin activity increased in an opposite trend to the fall of sodium. BUN and creatinine reached their highest levels in hypertensive patients two days after the peak of the crisis. Autopsies were performed on 23 patients who succumbed to the injury: eleven of them (48%) were hypertensive and had marked hypertrophy of left and right heart ventricles and of the adrenal glands when compared to the normotensive burn subjects. The cells of the zona fasciculata and the zona glomerulosa of the adrenal glands were very compact at histologic examination thus suggesting hyperactivity. This data shows that the incidence of hypertension in burn subjects is twice as high as that of the US population. Further studies of the renin-angiotensin-aldosterone system and the adrenal cortical function are indicated by the changes in plasma renin activity and the glandular weight and morphology seen at autopsy.
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PMID:Incidence of post burn hypertensive crisis in patients admitted to two burn centers and a community hospital in the United States. 15 92

Endocrine activity in patients with essential hypertension was studied by measuring the urinary excretion of catecholamines, prostaglandin E (PGE) and cyclic adenosine monophosphate (cAMP). Simultaneously, plasma renin activity, concentrations of serum sodium, potassium, blood urea nitrogen (BUN) and creatinine were determined. Systolic blood pressure and BUN increased progressively with age until the sixth decade. Urinary excretion of norepinephrine was correlated with the systolic blood pressure. In contrast, plasma renin activity and urinary excretion of PGE decreased progressively with the increase in systolic blood pressure. Although the cause of essential hypertension is not known, it is suggested that hypertension accelerates the aging process in the kidney and thus decreases renal PGE synthesis. This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. A decrease of PGE may also potentiate the vasopressor action of norepinephrine.
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PMID:Changes in hormonal activities relative to the severity of essential hypertension. 21 51

To test the influence of an inhibitor of angiotensin-converting enzyme, teprotide (SQ 20881), we administered it to seven patients with essential hypertension and normal renal function and nine with an unequivocal reduction in creatinine clearance, caused by bilateral renal-artery stenosis in two and by essential hypertension in seven. Despite the fall in blood pressure (112.7 +/- 4.5 to 100.3 +/- 3.9 mm Hg, mean +/- S.E.M., P less than 0.01), there were prompt increases in both creatinine clearance (95.9 +/- 10.5 to 109.9 +/- 9.5 ml per minute per 1.73 m2 of body-surface area, P less than 0.01) and sodium excretion (17.0 +/- 5.9 to 31.7 +/- 7.2 mumol per minute, P less than 0.01) in patients with essential hypertension. The increase in glomerular filtration rate was most striking, averaging 33 per cent (66.0 +/- 10.3 to 88.0 +/- 9.2 ml per minute per 1.73 m2, P less than 0.001) in patients in whom an initial reduction was evident and hypertension was more severe. These observations suggest that a functional element, perhaps involving angiotensin-mediated renal vasoconstriction, frequently has a role in the reduction in glomerular filtration rate that occurs in essential hypertension. This class of agent may improve renal excretory function as it controls hypertension.
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PMID:Increased glomerular filtration rate after converting-enzyme inhibition in essential hypertension. 22 9

Radiation injury to arteries can represent a significant complication of therapeutic irradiation, even when the dosage used has not been excessive as judged by approved protocols. Children in whom therapeutic abdominal irradiation has been used should be monitored indefinitely for the development of hypertension. The presence of hypertension in such children with normal blood urea nitrogen (BUN) and creatinine, and without proteinuria, should prompt investigation for a renovascular lesion. Standard bypass procedures are usually effective, although the long-term success may be compromised by continuing changes in affected vessels.
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PMID:Postradiation renovascular hypertension. 23 3

The theoretical background for a conservative therapeutic treatment of uremia is described, with illustrative results from preliminary clinical trials in 10 patients and 10 normal reference subjects. The proposed treatment focuses upon the patient's gastrointestinal tract--the normal site for metabolism of both exogenous (dietary) and endogenous (recycled) protein--enabling it to behave like the rumen of the cow. The objective is to induce the uremic's organism to utilize its own "waste" substances. The patient swallows enterosoluble capsules containing specifically adapted enzymes (immobilized or free) from apathogenic soil microorganisms. These are pre-adapted to convert urea, creatinine, uric acid, guanidino derivatives, and other nonprotein nitrogen compounds (NPN). The enzymes utilize many other substances, in particular ammonia, potassium, phosphorus, and several other factors potentially dangerous for the uremic. The enzymes apparently cleave vasoconstrictatory peptides in the intestines. In the course of the therapy, renoparenchymal hypertension decreased significantly, and increased again when the regimen was interrupted. The results from the present studies are in full accord with the information published in the relevant fields. The time appears ripe for large-scale trials of the therapeutic regimen outlined, especially as many commercial microbial enzymes already have a long history of safe use in food processing.
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PMID:Bacterial enzymes in uremia management. 27 91

The prevalence of clinical and sub-clinical occlusive arterial disease and of risk factors implicated in the pathogenesis of arteriosclerosis was assessed in 21 patients with chronic renal failure, 27 on maintenance haemodialysis and 51 renal allograft recipients. Clinical occlusive arterial disease was present in 27 patients, and sub-clinical arterial disease in 34. Myocardial infarction, cerebral thrombosis and lower limb arterial thrombosis had occurred only in the transplant recipients; these patients had, however, been followed for a longer period of time than the other two groups. In the allograft recipients, the cumulative incidence of any occlusive arterial disease was 416 per 1000, and that of coronary heart disease was 267 per 1000 at six years. Hypertension was present in 76 per cent of patients prior to renal replacement therapy. Following institution of definitive therapy, hypertension was of shorter duration and less common in haemodialysis patients than in renal transplant recipients. Uraemic and haemodialysis patients with occlusive arterial disease had required antihypertensive medication for significantly longer than those free of arterial disease. Transplant recipients with hypertension had a greater mean serum creatinine, were receiving a larger maintenance dosage of corticosteroids and less frequently had undergone prior bilateral nephrectomy than those transplant patients without hypertension. Serum lipid levels were elevated in 62 per cent of patients. In the uraemic and haemodialysis patients hypertriglyceridaemia was the predominant abnormality while in the transplant recipients combined hypertriglyceridaemia/hypercholesterolaemia was more frequent. Despite regular aluminium hydroxide therapy 81 per cent of uraemic and haemodialysis patients had a calcium X phosphate product higher than normal. Arterial and/or soft tissue calcification as demonstrable in 20-38 per cent of patients within each group, but could not be related to the calcium X phosphate product of radiographic evidence of hyperparathyroidism. Glucose intolerance was present in 71 per cent of the uraemic and haemodialysis patients and 33 per cent of the transplant recipients. Hyperuricaemia, cigarette smoking, obesity and a sedentary existence were also prevalent. The majority of patients had several risk factors implicated in the pathogenesis of arteriosclerosis. Occlusive arterial disease is a major problem in patients with end stage renal disease, being no less common after transplantation than with long-term maintenance dialysis. The aetiology is multifactorial.
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PMID:Occlusive arterial disease in uraemic and haemodialysis patients and renal transplant recipients. A study of the incidence of arterial disease and of the prevalence of risk factors implicated in the pathogenesis of arteriosclerosis. 32 93


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