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

The clinical course of diabetic nephropathy was evaluated in 150 patients and the effect of hemodialysis in 68 of them. Proteinuria was the first sign of renal disease. Once renal dysfunction becomes evident, there is a rapid deterioration leading to dialysis within 3.0 +/- 0.2 years. Hypertension and circulatory congestion are common complications. The hypertension is probably volume dependent. Retinopathy was not invariably present at the onset of renal insufficiency but appeared with progression of renal failure. The course during hemodialysis was complicated by continued progression of diabetic vascular disease manifested by vascular access difficulties, worsening of retinopathy and blindness, and cardio- and cerebrovascular deaths. Mortality was higher than in nondiabetic dialysis patients.
Nephron 1978
PMID:Diabetic nephropathy: clinical course and effect of hemodialysis. 64 44

15 patients who had benign, uncomplicated essential hypertension, were treated with chlorthiazide (500 mg twice a day) with or without propranolol (10--20 mg 4 times a day), and the effect of the treatment on plasma renin activity (PRA), urinary aldosterone excretion, total body potassium (TBK) and plasma sodium and potassium was evaluated. TBK depletion was significant mathematically (more than 5% of TBK lost) in 7 patients, but not significant physiologically (less than 15% of TBK lost) in any except in one, who may have had other reason for TBK depletion. Although propranolol prevented the increase in PRA and aldosterone excretion, it did not prevent the modest TBK depletion. Dietary potassium intake may have some importance in the maintenance of normal body potassium during chronic treatment with thiazides for hypertension.
Nephron 1978
PMID:The renin-aldosterone system and thiazide-induced depletion of total body potassium in essential hypertension. 71

We have investigated the influence of renal mobility on both renal blood flow and glomerular filtration, in order to evaluate its role as a potential intermediate cause of hypertension. In 25 untreated patients we compared between recumbent and upright position the relative change in the following five parameters: effective renal plasma flow (ERPF), glomerular filtration rate (GFR), renal mobility, peripheral plasma renin activity (PRA) and blood pressure. We found a positive correlation between the degree of renal mobility and an observed decrease in ERPF. On the other hand, no relation was found between the former and an observed decrease in GFR. The PRA appeared to rise following the decrease of the ERPF. These observations suggest that renal mobility adds to the orthostatic reduction in renal blood flow.
Nephron 1978
PMID:Nephroptosis and kidney function. 74 99

The hemodynamic mechanism of the hypotensive effect of propranolol was studied by quantitative radiocardiography in 8 patients with dialysis-resistant hypertension. Propranolol treatment brought about a decrease in mean arterial pressure and peripheral vascular resistances. The cardiac index was slightly reduced only in the early stage of the treatment. No significant difference was found between patients on treatments lasting longer than 3 months and patients with dialysis-controlled hypertension. The results show that propranolol can be used safely as the sole antihypertensive agent in patients with dialysis-resistant hypertension.
Nephron 1978
PMID:Chronic hemodynamic effects of propranolol treatment in dialysis-refractory hypertension. 74 Jan 3

High plasma renin activity (PRA) was found in 16 of 42 randomly selected nonuremic systemic lupus erythematosus (SLE) patients. Mild hypertension was present in 3 of the 16.6 high-PRA and 10 normal-PRA patients were admitted to a metabolic ward. Salt restriction produced a disproportionate rise in both PRA and aldosterone, a decrease in glomerular filtration rate (GFR) and a slightly greater negative sodium balance in the group with high PRA. Potassium excretion was less than intake in both groups. Balance studies were performed in 6 additional high-PRA patients before and during indomethacin administration (150 mg/24 h). PRA and aldosterone were markedly suppressed by indomethacin. UnaV was significantly greater than in the control period despite of the 28% reduction in GFR. These results suggest that high PRA is secondary to impaired distal tubular sodium reabsorption. Such a defect could be responsible for the relatively low frequency of hypertension in lupus nephritis.
Nephron 1978
PMID:Normotensive hyperreninemia in systemic lupus erythematosus. An indicator of tubular dysfunction. 74 33

From 1955 to 1977, 27 pediatric patients underwent surgical treatment for renovascular hypertension. Renal artery disease was most commonly caused by intimal or perimedial fibroplasia and occurred bilaterally in 7 patients. Overall results were 16 patients cured (59%), 5 patients improved (19%) and 6 failures (22%). The best results were obtained in children with unilateral renal artery stenosis. In recent years, ablative surgery has been largely supplanted by reconstructive vascular procedures in the treatment of this disease in children. Autogenous vascular bypass grafts have been most successful and aortorenal reimplantation may occasionally be employed. Renal autotransplantation should be reserved for children with the middle aortic syndrome or multiple lesions involving the branches of the renal artery. Splenorenal bypass and segmental resection with renastomosis have yielded poor results and are best avoided in this age group. Primary nephrectomy should only be performed in patients with renal atrophy or uncorrectable branch vessel disease. Renovascular hypertension in children is a potentially curable disease and revascularization with preservation of renal function should be the combined objectives of surgical therapy in the most cases.
Nephron 1978
PMID:Stenosing renal artery disease in children: clinicopathologic correlation and results of surgical treatment. 74 36

Renovascular hypertension developed in an anephric 37-year-old patient after he received a cadaveric renal transplant from a 2-year-old donor. Despite adequate homograft function, a transplant nephrectomy was perfomed because of intractable, lifethreatening hypertension. There was relative stenosis throughout the course of the transplanted renal artery. Pathologic examination of the kidney did not demonstrate evidence of technical failure or immunological or hypertensive damage. Atrophic changes in the media of the renal artery may have resulted from radiation damage. The hypertension appears to have been caused by disproportionate growth between the parenchyma in the hypertrophying pediatric homograft and its renal artery.
Nephron 1976
PMID:Intractable renovascular hypertension in an adult recipient of a pediatric cadaveric renal transplant. 78 46

1. Noradrenaline, adrenaline and alpha-methylnoradrenaline administration into the nucleus tractus solitarii (NTS) of anaesthetized rats decreased blood pressure and heart rate in a dose-dependent fashion. 2. Bilateral injections were effective in lower doses than unilateral administration. alpha-Methylnoradrenaline given bilaterally produced hypotension in a dose of 0-08 nmol whereas after unilateral injection a dose of 0-32 nmol was needed to obtain the same degree of hypotension. 3. Electrical stimulation of the NTS caused hypotension and bradycardia. Conversely, bilateral electrolytic lesions or deafferentation of the NTS led to acute hypertension. Chronically such lesions caused neurogenic hypertension. 4. In spontaneously hypertensive rats increased concentrations of noradrenaline, adrenaline and dopamine were measured in the part of the NTS located just caudal to the obex (A2 region).
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PMID:Brain-stem structures and catecholamines in the control of arterial blood pressure in the rat. 79 55

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge. 2. The same procedure was repeated in the same subjects 3--4 days later after pretreatment with oxprenolol. 3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged. 4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values. 5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.
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PMID:Effect of oxprenolol on catecholamines and plasma renin activity: acute response to frusemide in hypertensive patients. 80 48

Using specific anesthetic agents, permanent segmental occlusion of the proximal middle cerebral artery (MCA) causes ischemic infarction limited to the putamen and other deep hemispheral structures in primates. Using this model, 25 rhesus monkeys were subjected to acute arterial hypertension before, during and up to 5 days after onset of MCA occlusion in order to reevaluate the possible role of the ischemic process in pathogenesis of cerebral hemorrhage. Norepinephrine infusion induced prompt rapid rise in mean arterial pressure (MAP) and intracranial pressure (ICP) limited to the duration of infusion. This procedure produced acute ischemic lesions which were totally bland but topographically more extensive than untreated controls; in chronic lesions, however, deep nuclear masses showed hemorrhagic infarction. Animals given 5% CO2 air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilan hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematoma involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantiative changes in lesion size. In the vasoproliferative stages of mature infarction, MAP elevation induced by a cerebral vasoconstrictor caused hemorrhagic infarctions while cerebral vasodilation caused intracerebral hematomas.
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PMID:Primate model of cerebral hematoma. 82 36


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