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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Saralasin and converting enzyme inhibitors SQ 20881 and captopril induced increases in plasma renin activity to greater than 14 ng h-1 ml-1 in 43 out of 44 patients with untreated renovascular hypertension when studied in the seated position and on normal sodium intake. This degree of response was absent in patients with normal-renin essential hypertension and present in only three out of 26 with high-renin essential hypertension. 2. Reductions of greater than approximately 9% in diastolic pressure in response to these three drugs occurred regularly in renovascular hypertension (95%) but also frequently in high-renin (65%) and normal-renin (26%) essential hypertension. 3. Prior sodium depletion abolished the specificity of the renin and depressor responses to angiotensin blockage for renovascular hypertension. 4. Some patients with bilateral renovascular and all with malignant hypertension also exhibited these responses to angiotensin blockade that are characteristic of unilateral renovascular hypertension.
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PMID:Reactive hyper-reninaemia to angiotensin blockade identifies renovascular hypertension. 23 24

Arterial intimal thickening is common in the end-stage kidneys of patients maintained on hemodialysis. We measured the intimal thickening in patients dialyzed for varying periods and in patients with the malignant phase of essential hypertension and with scleroderma-associated renal failure. The ratio of intimal area to medical area in intrarenal arteries was used as a measure of intimal thickening. In the dialysis groups, intimal thickening was relatively constant in arteries of all sizes and correlated with duration of dialysis, particularly in larger arteries. In the malignant hypertension and scleroderma groups, the intimal thickening was greatest in arteries less than 200 mu in diameter and least in those over 500 mu in diameter. There was much less intimal thickening in arteries of all sizes in kidneys of patients with end-stage polycystic disease than in other end-stage kidneys from patients with a similar diastolic blood pressure and similar duration of dialysis. We believe that the intimal thickening in dialyzed patients is probably a disuse type of change and may be related to reduction in the area of the renal microvascular bed.
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PMID:A morphometric study of arterial intimal thickening in kidneys of dialyzed patients. 45 27

The pathological changes in blood vessels observed in primary (essential hypertension) are similar to those seen in secondary hypertension due to renal disease or other causes. In benign hypertension, the major changes are in the small arteries and arterioles especially in the kidney. Interlobular arteries exhibit intimal thickening and duplication of the elastic lamina (elastosis) and there is hyaline change in the media of many arterioles. In some respects these changes are an accentuation of vessel ageing. Malignant hypertension usually presents in a younger age group (35--50 years) and is characterized pathologically by fibrous endarteritis in the interlobular arteries of the kidney and fibrinoid necrosis in the walls of a proportion of the efferent glomerular arterioles. Similar vessel changes are seen in other organs but many of the pathological changes in the heart and brain of patients with benign hypertension are related to the accentuation of arterosclerosis. There is an increased mortality from cardiac failure, myocardial infarction, cerebral haemorrhage and subarachnoid haemorrhage due to ruptured berry aneurysms in patients with benign hypertension. Although there is ischaemic damage to the kidneys in benign hypertension, death from renal failure is uncommon. Severe ischaemic damage to renal glomeruli and renal failure does, however, occur in malignant hypertension.
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PMID:Vascular pathology in hypertension. 46 85

A follow-up was made of 69 patients diagnosed as having malignant hypertension during 1969--76, essential in 26, secondary in 39 and unclassified in 4. A clear male dominance was seen (41 men, 28 women), particularly in the group with essential hypertension (18 men, 8 women). The mortality in this series was less than in previously published series. Thus, the 5-year survival rate was 75% in the patients with essential and 72% in those with secondary hypertension. In part this was due to haemodialysis and renal transplantation. The importance of renal function at the time of diagnosis was evident in this study. In most patients with essential hypertension and serum creatinine levels below 300 mumol/l, renal function could be maintained or improved when antihypertensive treatment was instituted, whereas progression of the renal damage was seen in those with serum creatinine levels above 300 mumol/l in spite of antihypertensive treatment with 3 or more drugs. The incidence of new cases of malignant hypertension tended to decrease during the observation period, particularly as regards essential hypertension.
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PMID:Malignant hypertension--improving prognosis in a rare disease. 53 11

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.
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PMID:Serum uric acid and the renin-angiotensin system in hypertension. 65 66

Fourteen autopsied cases of malignant nephrosclerosis were classified into 6 of pure form in which syndrome of malignant hypertension developed from the beginning of the disease, and 8 of exacerbated form with appearance of the syndrome in the course of essential hypertension. Pathohistological study of these cases elucidated the differences in histologic manifestations between pure and exacerbated forms of malignant nephrosclerosis as to which little had been known as yet. In the pure form arterioles and small arteries characteristically demonstrated acute or recent lesions such as fibrinoid necrosis and hemorrhage into intima, and intimal cellular hyperplasia of somewhat longer duration, whereas in the exacerbated form coexistence of vascular lesions of various intensities and durations, acute (fibrinoid necrosis and hemorrhage), intermediate (intimal cellular hyperplasia) to chronic (sclerosis and lamellar elastosis), and superposition of more recent vascular lesions on more advanced or older ones were noted. Superposition of vascular alterations was interpreted to be not necessarily specific for exacerbated form but histologic manifestation of recurrence which is liable to be the case more frequently in exacerbated form than in pure form in the longer course of essential hypertension or of malignant hypertension. Some other related problems were also considered and discussed.
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PMID:Pathology of malignant nephrosclerosis with special reference to the difference between histologic manifestations of pure and exacerbated forms. 69 19

The effect of indomethacin or placebo on aldosterone, plasma renin activity (PRA), sodium excretion, and urinary prostaglandin (PG) levels was investigated in five hypertensive subjects in 100 mEq sodium balance who had experienced malignant hypertension with a disturbance of their renin-aldosterone relationship in the past. Indomethacin significantly lowered aldosterone levels by 43%, PRA by 58%, 24-hour sodium excretion by 49%, and urinary PG excretion, an indicator of renal PG synthesis, by 67%. Angiotensin infusion increased aldosterone to the same level before and after treatment with indomethacin. Similarly, in normal subjects in 150 mEq sodium balance, indomethacin lowered PRA by 47%; sodium excretion fell by 33%, and urinary prostaglandin E (PGE) excretion, by 55%. The acute elevation in PRA 10 minutes after intravenous furosemide was completely abolished by indomethacin. Five subjects with essential hypertension were classified as normal renin hypertensives according to their response to orally administered furosemide. Indomethacin pretreatment resulted in 60% reduction of PRA following furosemide, and three of these subjects now fell into the low renin category. Studies in vitro demonstrated that indomethacin has no effect on the renin-renin substrate interaction. Thus, indomethacin lowers PRA concomitantly with a reduction in renal PG synthetase activity. Whether indomethacin inhibits renin release by an intrarenal, PG-related mechanism or secondarily via sodium retention is discussed.
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PMID:Suppression of plasma renin activity by indomethacin in man. 82 75

Eighteen patients with advanced or malignant hypertension due to essential hypertension, systemic lupus erythematosus or chronic glomerulonephritis were infused intravenously with 1-Sar-8-Ile-Angiotensin II, a competitive antagonist of aniotensin II. The spectrum of responses was broad from a mild elevation to a marked fall in blood pressure. The changes in mean blood pressure caused by this peptide showed a significant correlation with the level of peripheral plasma renin activity immediately before the infusion (r=0.5652, p less than 0.02). This peptide infusion reduced blood pressre in 12 patients (responders), but not in 6 (non-respnders). There were no differences with age, sex and severity of hypertension except for the level of peripheral plasma renin activity between the two groups. Our retrospective study showed that in 12 responders propranolol reduced blood pressure to near the normal level, while in 6 non-responders furosemide induced similar depressor response. It is concluded that the vasodepressor effect of this peptide correlates with the levels of peripheral plasma renin activity and that the responses to this drug can be used as a guide for the selection of effective antihypertensive drugs.
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PMID:Clinical evaluation of angiotensin II antagonist in advanced hypertension. 88 41

Plasma renin activity (PRA) was determined in 48 patients with diabetes mellitus in sodium balance on a 10-20 mEq. Na diet. Nine were normotensive (group I), 11 11 were hypertensive without diabetic nephropathy (group III). Results were compared with those in 16 normal subjects and 49 nondiabetic patients with essential hypertension in similar Na balance. Mean supine PRA did not differ significantly among groups I and II, normal subjects, and patients with essential hypertension. Group III diabetics had a supine PRA of 2.4 +/- 0.4 ng./ml./hr. (x +/- S.E.M.), significantly lower than the other diabetic groups (P less than 0.005) and normal subjects (P less than 0.05). Upright PRA was 12.8 +/- 2.2 in group I diabetics, similar to that in normal subjects (13.3 +/- 2.3), and 8.1 +/- 1.4 in group II diabetics, similar to that in essential hypertensives (6.8 +/- 0.8). In group III diabetics, upright PRA was 4.0 +/- 0.5, significantly lower than that in any other group. These results suggest that (1) PRA is normal in normotensive diabetics, (2) upright PRA in diabetics with hypertension but no nephropathy is similar to that in essential hypertension, and (3) patients with diabetes, hypertension, and nephropathy have "low renin hypertension," explaining the virtual absence of malignant hypertension in this group. Although the major mechanism for this low PRA may be volume expansion, indicating the need for potent diuretics, other mechanisms include hyalinization of the afferent arteriole, decreased cathecholamine stimulation of renin release, and inadequate conversion of prorenin to renin.
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PMID:Plasma renin activity and hypertension in diabetes mellitus. 97 6

Whether a person is medically fit to engage in sports depends not only on his or her present state of health but also on his or her previous medical history, age, personality, and of course, the nature of the particular sport in question. Anyone that feels fit, is physically in good condition, abstains from tobacco, alcohol and other intoxicant stimulants, and passes a thorough medical examination is healthy and fully capable of taking part in any sport whatever. Participation in any form of sport, on the other hand, is absolutely contra-indicated for persons suffering from severe or malignant hypertension, inflammatory or bacterial heart disease, severe angina pectoris - especially with an attendant risk of myocardial infarction - or haemodynamically significant arrhythmias that manifest themselves during, or are aggravated by, physical exertion. Physical activity is generally deleterious in patients with advanced pulmonary disease and chronic cor pulmonale, severe decompensated heart failure or severe renal insufficiency. Severe intercurrent infections also constitute an absolute contra-indication for sport. Between these two extremes of absolute fitness and absolute unfitness there are many intermediate states, e.g. diseases like essential hypertension (WHO Stages I and II), coronary disease and peripheral arterial circulatory disorders, in which patients can derive considerable benefit from properly chosen and carefully graded sporting activity.
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PMID:[Medical fitness for sports, with particular reference to cardiovascular conditions]. 102 Apr 74


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