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

The purpose of the present study was to examine the influence of different sodium loads on renin release in the hypertensive and normotensive state of chronic renal failure. Blood pressure (BP), plasma renin concentration (PRC) and exchangeable sodium (NaE) were measured in eighteen patients with advanced chronic renal failure, nine hypertensives and nine normotensives, and in seven normal subjects (a) 6 days after a fixed sodium intake of 10 mmol/day, and (b) 6 days after a fixed sodium intake of 150 mmol/day. Mean NaE was 14-19% higher in the hypertensives compared with the normotensives and values of NaE correlated significantly to values of mean BP. No significant differences were present in PRC between the groups of patients and controls on either of the sodium regimens and no correlation was found between BP and PRC. However, average decreases of PRC in the hypertensives on high sodium intake, 33-34%, were significantly lower than the corresponding values of 69-71% in the normotensive patients and controls, respectively. Furthermore, the percentage changes of PRC on high sodium intake correlated significantly to mean BP as well as to NaE. These results suggest that renin release is relatively unresponsive to different sodium intakes in hypertension following chronic renal failure. This alteration in renin release may contribute to the maintenance of hypertension in chronic renal failure, PRC being "inappropriately' increased in relationship to the sodium excess.
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PMID:The influence of different sodium loads on renin release in hypertensive and normotensive states of chronic renal failure. 14 27

Intra-cisternal clonidine (3 microgram/kg) reduced hypertension and cardiac acceleration after defrenation in dogs, but did not act in intra-venous infusion (10 microgram/kg). The renin activity was not modified. Clonidine was always inactive on hypertension after stimulation of visceral afferences or after injection of potassium cyanidine. These results show that a central mechanism was implied in the anti-hypertensive action of clonidine.
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PMID:[Effect of clonidine on three types of experimental hypertension and on plasma renin activity in dogs]. 15 Aug 95

Twenty-four patients with persisting hypertension after renal artery reconstruction were re-investigated 1--8 years after surgery. They underwent renal arteriography, determination of plasma renin activity, renography and renal function studies in order to find the causes of the postoperative hypertension. Restenosis was found in 6 patients, in 3 of whom it was of functional significance according to the positive renin tests (renin ratio greater than 1.5). Positive renin tests were found in 2 other patients. One had occlusion of a renal artery branch and the other hypoplasia of the kidney due to chronic nephritis. No explanation of the persisting hypertension could be found in 19 patients at re-examination. In 10 of them, however, biopsy from the affected kidney obtained during operation showed nephrosclerosis, which may explain the outcome. Fourteen of the 19 patients had negative renin tests preoperatively. These negative tests indicate that renal artery stenosis was not the only cause of hypertension. It may be concluded that the renin test is of the utmost value in the selection of patients for renal artery reconstruction and should always be considered. A biopsy from the contralateral kidney may be necessary in order to detect other causes of hypertension than renal artery stenosis. The importance of re-investigating patients with persisting hypertension is confirmed by the present study.
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PMID:Persisting hypertension after renal artery reconstruction. A follow-up study. 15 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

Young, unilaterally nephrectomized, female Sprague-Dawley rats were given daily sc injections of 19-nor-deoxycorticosterone acetate (19-nor-DOCA) in oil at a dosage of 100 micrograms/day for 21 days and twice that amount for a further 11 days. One group drank distilled water and another drank 1% NaCl solution. Comparable control groups received oil injections. Another group received DOCA at the same steroid dosage and drank saline. Both 19-nor-DOCA-treated groups rapidly became hypertensive and developed cardiac hypertrophy, as did those given DOCA and saline. Saline consumption was greater in rats receiving 19-nor-DOCA, than in those given DOCA. Rats injected with 19-nor-DOCA and given water to drink showed enhanced growth and developed thymus enlargement and displayed hypokalemia and a reduction in both serum renin activity and corticosterone concentration. Plasma sodium concentration was not affected by any form of treatment. Clearly, 19-nor-DOCA is a potent mineralocorticoid and hypertensogenic agent. Since the parent steroid is known to be present abundantly in the urine of rats with regenerating adrenal glands, although circulating amounts have not yet been ascertained in that circumstance, it may be etiologically involved in adrenal regeneration hypertension, which such rats are prone to develop.
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PMID:Influence of 19-nor-deoxycorticosterone on blood pressure, saline consumption, and serum electrolytes, corticosterone, and renin activity. 15 70

An unusual case of orbital tumor with high renin content and severe hypertension is described. The patient was a 15-year-old girl with juvenile hypertension (200-140 mmHg) associated with right exophthalmos and hypokalemia. The patient showed extremely high levels of plasma renin activity and plasma aldosterone concentration. No difference was present in plasma renin activity from either side of the renal veins. Preoperatively, hypertension responded to treatment with spironolactone. The tumor could not be completely removed because of intracranial metastasis and infiltration, and the hyperreninemia and secondary hyperaldosteronism persisted. The renin content in the orbital tissue was 1,403-2,225 ng/angiotensin I generated/h/g wet weight of tissue. The postmortem histopathologic diagnosis was orbital hemangiopericytoma. This is the first case of extrarenal (ectopic) renin-secreting (or -producing) hemangiopericytoma of the orbital origin. Furthermore this case is worthy of note in the point of view of the presence of the extrarenal renin-angiotensin system, particularly in the brain.
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PMID:A case of ectopic renin-secreting orbital hemangiopericytoma associated with juvenile hypertension and hypokalemia. 15 52

Increased arterial pressure is obviously the major stimulus to cardiac hypertrophy in hypertension. However, different studies suggest that in addition to the pressure load, other factors could play participating roles in determining the degree of ventricular hypertrophy in response to the hypertensive disease as well as the degree of its reversal after control of arterial pressure. These other mechanisms include genetic factors and concimitant processes such as aging and the presence of cardiomyopathy or other disease. Two neurohumoral influences, namely, the adrenergic and the renin-angiotensin systems, may also participate, and the early evidence supporting these possible contributing factors is cited. Further studies are needed to determine the relative importance of each of these factors in different types of hypertension and in their response to different modes of antihypertensive therapy.
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PMID:Is arterial pressure the sole factor responsible for hypertensive cardiac hypertrophy? 15 71

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

An investigation of the relationship between nephrotensin and the renin angiotensin system was carred out. Nephrotensin was found in the plasma of rats with renal clip hypertension and with chemically induced kidney damage. There was no demonstrable correlation between presence of nephrotensin and plasma renin activity, and the pressor activity of nephrotensin was not altered by previous immunization of test animals with angiotensin II nor by pretreatment with angiotensin I converting enzyme inhibitor. These results indicate that nephrotensin is different from the components of the renin-angiotensin system.
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PMID:Differentiation of nephrotensin from the renin angiotensin system. 16 47

Big renin, a relatively inactive renin which possesses a molecular weight larger than that of normal plasma or renal renin, has been demonstrated by gel filtration in certain human plasma, tumor extracts, and amniotic fluid. Big renin was not present in normal plasma or kidney extracts. Plasma from 3 hypertensive patients with nephropathy contained chiefly big renin. Varying proportions of both big and normal renin activity were present in plasma of other patients with hypertension and proteinuria. The renin present in amniotic fluid, which increased in activity following exposure to acid pH, was shown to be big renin in two patients. Large amounts of circulating big renin apparently can cause hypertension in patients with Wilms' tumors. Furthermore, the relatively inactive big renin may replace normal plasma renin in some patients, resulting in low plasma renin activity.
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PMID:Occurrence of big renin in human plasma, amniotic fluid and kidney extracts. 16 87


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