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

Prazosin was used in combination with other antihypertensive drugs in the successful management of hypertension in seven patients with chronic renal failure and six renal transplant recipients, also with chronic renal failure. The addition of small doses of prazosin (mean 3 mg/day) to the antihypertensive regimen produced significant falls in systolic and diastolic blood pressures in both the lying and standing positions. The standing blood pressures were significantly lower than the lying blood pressures during prazosin treatment. Neither the mean blood urea concentrations nor the mean plasma creatinine concentrations changed significantly during prazosin administration. Chromium-51 edetic acid clearances did not change significantly during prazosin treatment in the seven patients in whom it was measured. Severe symptomatic postural hypotension occurred in one patient a week after starting prazosin 3 mg/day. This hypotensive episode was associated with a transient and reversible deterioration in renal function. Another patient developed a rash while on prazosin but it was probably related to propranolol rather than prazosin. Prazosin is thus an effective antihypertensive drug in patients with chronic renal failure, and it may be used with a variety of other drugs. It should be used cautiously, however, since patients with chronic renal failure may respond to small doses, and significant postural falls in blood pressure may result. There was no evidence that the use of prazosin resulted in progressive deterioration in the residual renal function of the patients with chronic renal failure.
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PMID:Use of prazosin in management of hypertension in patients with chronic renal failure and in renal transplant recipients. 81 12

Indomethacin inhibits the synthesis of prostaglandin and the release of renin. These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
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PMID:The effect of indomethacin blockade of prostaglandin synthesis on blood pressure of normal rabbits and rabbits with renovascular hypertension. 83 Apr 37

A previously normotensive 24-year-old black man developed malignant hypertension and azotemia. The patient was found to have bladder outlet obstruction due to urethral stricture. Transurethral dilation resulted in brisk improvement in renal function and rapid lowering of blood pressure in association with minimal diuresis. On follow-up one year later, while he was not receiving medications, the blood pressure was 120/70 mm Hg and the creatinine clearance was 150 ml/min. A kidney biopsy specimen showed minimal residual pathologic abnormalities in the renal arteries and arterioles. The renin-angiotensin system was probably involved in the maintenance of the hypertension, in view of the elevated peripheral plasma renin activity on admission. This represents a rare case of hypertension due to urethral stricture. Despite rapid progression to azotemic malignant hypertension, urethral dilation restored the blood pressure and renal function to normal.
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PMID:Reversible malignant hypertension and azotemia due to urethral stricture. 84 54

The role of renin was assessed in moderate and severe one-clip, two-kidney hypertension in rabbits during normal and high Na intake. Severe hypertension occurred with high levels of plasma renin and creatinine and with extracellular volume depletion. In this group, hypertension was significantly reduced by the 1-hour intravenous infusion of 1,000 ng/kg of an angiotensin II antagonist or by correcting the volume depletion with a high Na intake, which also decreased renin activity and creatinine. The infusion of the antagonist after a high salt diet failed to decrease blood pressure further. Moderate hypertension occurred with plasma levels of renin that were slightly below normal and with no significant abnormalities in extracellular volume depletion or creatinine. In this group, the administration of an angiotensin II antagonist or a high salt diet did not affect any of the three parameters. In normotensive controls, the blood pressure level was not affected by either the angiotensin II antagonist or the high salt diet, despite a reduction in plasma renin activity. Thus, high levels of renin are important in maintaining severe hypertension, and these increased levels probably are accompanied by a concomitant depletion of extracellular volume. Correction of the extracellular volume depletion by a high salt diet is followed by a decrease in renin activity and in blood pressure. In contrast, renin activity does not seem to be important in maintaining moderate hypertension, the pathogenetic mechanism of which remains to be elucidated.
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PMID:The effect of high sodium intake and angiotensin antagonist in rabbits with severe and moderate hypertension induced by constriction of one renal artery. 87 Feb 27

The mechanism of the chronic phase of one-clip, two-kidney hypertension was investigated in 23 dogs. Mean arterial pressure (MAP), renal hemodynamics, and arterial and renal venous plasma renin activity (PRA) were studied before and at 1 and 3 months after graded, unilateral renal artery constriction. In the dogs that demonstrated sustained hypertension, the magnitude of changes in MAP, renal hemodynamics, PRA, and renal renin secretion correlated with the severity of renal artery constriction. In dogs with severe constriction (group 3, 78-86% renal blood flow reduction), MAP and arterial PRA were significantly elevated throughout. In groups 1 and 2 (0% and 50-56% renal blood flow reduction, respectively), although MAP remained significantly elevated, arterial PRA decreased to baseline values by 3 months. In group 3, there was an initial, apparent redistribution of ipsilateral renal blood flow, and prolonged reductions in ipsilateral renal plasma flow (RPF) and glomerular filtration rate accompanied by significantly increased creatinine clearance (CCreat) in the untouched kidney. Similar but less marked renal hemodynamic changes occurred in the other hypertensive dogs. All hypertensive dogs, regardless of degree of renal artery constriction, demonstrated significantly increased ipsilateral renal renin secretion and contralateral renin suppression. In three dogs that were studied 6, 12, and 16 months postconstriction, the high rate of ipsilateral renin secretion persisted throughout. Ipsilateral nephrectomy consistently resulted in rapid amelioration of the hypertension. These findings are in accord with a renal-dependent and probably renin-mediated mechanism for the maintenance of high blood pressure in the chronic phase of the one-clip, two-kidney dog model.
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PMID:Mechanisms of hypertension during the chronic phase of the one-clip, two-kidney model in the dog. 87 Feb 31

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.
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PMID:Symptoms and course of chronic hypokalemic nephropathy in man. 87 Feb 67

Study of 108 samples of amniotic fluid obtained between 28 and 42 weeks' gestation from 101 patients revealed that in normal pregnancies the creatinine concentration, lecithin/sphingomyelin (L/S) ratio and percentage of fat cells correlated better with the gestational age of the newborn--assessed by clinical criteria--than did the bilirubin and sodium concentrations. A creatinine concentration of 1.75 mg/dL or more, an L/S ratio of 4 or more and a fat cell percentage of 10 or more correlated significantly with a gestational age of 37 weeks or more. In abnormal pregnancies (those with obstetric or medical complications, or both) the mean creatinine concentration in the amniotic fluid was significantly less than expected for gestational age in fetal dysmaturity and greater than expected when the mother had diabetes. The mean L/S ratio in the amniotic fluid was elevated when the mother had hypertension or smoked and in cases of fetal dysmaturity or long interval between rupture of the membranes and delivery, whereas it was significantly lower than normal when the mother had diabetes. The mean bilirubin concentration in the amniotic fluid was significantly lower than normal when the mother had hypertension. When the mother had diabetes, maturity of the fetal lung, liver, skin and brain appeared to be delayed, according to the values for the amniotic fluid constituents.
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PMID:Estimation of gestational age from study of amniotic fluid and clinical assessment. 91 15

Nine patients with non-functioning kidneys and complete renal artery occlusion discovered on arteriographic investigation for hypertension underwent renal artery revascularization with successful restoration of renal blood flow. Of these patients 7 experienced recovery of renal function and 2 showed no evidence of improvement. One patient had a creatinine clearance of 38 cc per minute from the revascularized kidney 2 years postoperatively. Predictive determinants of salvageable renal parenchyma were the histologic evidence of intact viable glomeruli and the angiographic features of a rich perihilar collateral circulation in the presence of a proximal occlusion with a patent distal renal artery.
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PMID:Revascularization of the chronic totally occluded renal artery with restoration of renal function. 91 39

During a retrospective study of 100 patients who underwent renal biopsy because of pregnancy complicated by hypertension, we found 19 patients whom proteinuria exceeded 5.0 Gm. per 24 hours and an additional eight patients in whom excretion ranged between 3.5 and 5 Gm. per day. Of these 27 patients, 23 had the kidney lesion of pre-eclampsia, and three of them had superimposed hypertensive changes in the vasculature. The remaining four had other renal diseases. We located and re-examined 10 of the 23 pre-eclamptic women, 12 to 104 (mean, 36) months after delivery. Serum creatinine levels were normal in all but one, who was discovered to have polycystic kidney disease. During the same time period, we located the records of six women who had heavy proteinuria during gestation but were normotensive. Thus, at our institution, pre-eclampsia is the most common cause of the nephrotic syndrome in pregnancy. The frequency of nephrotic proteinuria in pre-eclampsia appears higher than previously suspected, but, despite this fact, recovery was complete in most instances.
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PMID:Nephrotic proteinuria with pre-eclampsia. 92 Jul 65

Hypertension occurring in patients with adult polycystic kidney disease (PKD) without substantially decreased glomerular filtration rate (GFRs) has not been sufficiently evaluated. Seven patients with bilateral PKD and serum creatinine clearances greater than 70 ml/min were studied to examine the roles of sodium retention and the renin-angiotensin system in their hypertension. These individuals demonstrated evidence of volume expansion and sodium-dependent hypertension. However, the renin-angiotensin system was not consistently depressed as a consequence, and two of the seven had significantly increased plasma renin activity values. It seems that patients with PKD who had normal GFRs retain rather than waste sodium and may become hypertensive. The contribution of the renin-angiotensin system is variable and seems to be a function of such factors as symmetry of the cystic involvement and the degree of intravascular volume expansion.
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PMID:Hypertension in polycystic kidney disease without renal failure. 92 44


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