Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Split renal function tests were studied in 41 patients with unilateral stenosis of the main renal artery in comparison with 36 subjects with essential hypertension. The two populations were matched for sex, age (39 +/- 10 vs 37 +/- 11 years (+/- 1 standard deviation) and systemic arterial pressure (193/114 +/- 29/15 vs 205/110 +/- 30/17 mmHg). The PAH clearance (CPAH) was decreased in essential hypertensives. The decrease was similar in the right (160.3 +/- 56.9 ml/min/m2) and left kidneys (158.7 +/- 45 ml/min/m2). The inulin clearance (Cin) was similar in both kidneys (35.2 +/- 12.5 vs 33.6 +/- 11.6 ml/min/m2). In addition, in essential hypertensive, CPAH was negatively correlated with blood pressure (p less than 0.01). In patients with renal artery stenosis, CPAH of the "stenotic" kidney was reduced (91.5 +/- 47.8 ml/min/m2) as well as Cin (22.9 +/- 9.3 ml/min/m2). In contrast, a significant increase in CPAH (194.1 +/- 63.8 ml/min/m2) and Cin (47.6 +/- 12.6 ml/min/m2) was observed in the contralateral kidney. Kidney function (CPAH and Cin) was not correlated with blood pressure in the "stenotic" kidney. CPAH and Cin of the non stenotic kidney were positively and significantly correlated with systemic arterial pressure (p less than 0.01). Cin was positively correlated with CPAH (p less than 0.001) in all kidneys in renovascular or in sustained essential hypertensives. However, in the contralateral kidney of renovascular hypertensives, a significant upward resetting of the correlation was observed. The Cin/CPAH was increased in the stenotic kidney (25.7 +/- 7.6%), as well as in the contralateral kidney (25.6 +/- 6.2%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of renal hemodynamics in 2 types of arterial hypertension, essential and renovascular, in man. Physiopathological implications]. 339 58

Mild hyperuricemia in patients with essential hypertension reflects early renal vascular involvement. This report describes a retrospective analysis of 28 patients with unilateral renal arterial disease and hypertension who underwent surgical treatment. Following surgical repair of the arterial lesion: systolic pressure decreased from 188 +/- 25 to 146 +/- 21 mm Hg (p less than 0.001); diastolic pressure decreased from 108 +/- 4 to 87 +/- 6 mm Hg (p less than 0.001), and serum uric acid and creatinine concentrations decreased from 7.0 +/- 1.1 to 6.1 +/- 1.4 mg/dL and from 1.3 +/- 0.3 to 1.0 +/- 0.3 (p less than 0.02 and p less than 0.03, respectively). The reduced serum potassium levels, reflecting hyperaldosteronism, increased after surgical treatment (p less than 0.003). The 28 patients were classified in three groups according to previous therapy: group I (14 patients) had been treated with a centrally active adrenergic agonist or a beta adrenergic receptor blocking agent; group II (7 patients) had been treated with a diuretic, and group III (7 patients) had never received antihypertensive therapy. Serum uric acid concentrations were similar in each of the three groups and decreased significantly in each group after correction of the renal artery stenosis. These data strengthen our previous observations and further suggest that serum uric acid concentration may be useful as an index of renal vascular involvement in hypertension.
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PMID:Serum uric acid in renovascular hypertension: reduction following surgical correction. 342 90

An estimation of renal secretion rates of PGE2 and PGF2 alpha, in parallel with renin-angiotensin-aldosterone system and catecholamines was performed on control subjects, essential hypertensive, and renovascular hypertensive patients. In essential hypertensive patients with normal plasma renin activity (PRA) and normal catecholamines level. We did not find any changes in the renal prostaglandin (PG) secretion rate as compared to the control subjects. Our results do not support the hypothesis that a reduction of PGE2 production is a specific feature of patients with essential hypertension. In renovascular hypertensive patients with unilateral renal artery stenosis we found: 1. High PRA in the renal plasma of the abnormal (with renal artery stenosis) kidney, and in peripheral plasma; 2. Decreased renal release of PGE2 from both kidneys, more distinct in abnormal kidney; 3. No changes of renal production of PGF2 alpha. The positive and negative correlation between renin-angiotensin system and renal PGs in physiological and pathological conditions was discussed.
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PMID:Humoral factors involved in the regulation of sodium-fluid balance in man. III. Renal prostaglandins and renin-angiotensin-aldosterone system in hypertensive disorders. 347 25

In the present study 25 patients with various forms of severe hypertension (essential hypertension: n = 12; renovascular hypertension: n = 11; unilateral small kidney: n = 2), which were treated with captopril for a mean control period of 34.9 months, were investigated. Reduction of mean blood pressure under captopril was comparable in all subgroups. However, patients with renovascular hypertension showed a significant increase in serum creatinine from 117 to 162 mumol/l (p less than 0.05) after 34.9 months, whereas in essential hypertensives even a slight decrease could be observed (113 vs. 111 mumol/l). Serum creatinine of the 2 patients with unilateral small kidney remained within the normal range. Changes in creatinine were markedly higher in cases with bilateral renal artery stenosis and/or in those with a very high initial plasma renin activity (greater than 15 ng/ml X 3 h). Our findings underline the necessity of cautious application of captopril in patients with renovascular hypertension.
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PMID:Captopril and kidney function in renovascular and essential hypertension. 352 86

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.
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PMID:Proteinuria in hypertension. 368 33

Posttransplant hypertension is an important risk factor for cardiovascular mortality and graft function. We performed metabolic studies in 35 hypertensive patients with well-maintained graft function on maintenance immunosuppressive drugs and in 17 normotensive control transplant recipients. The group of hypertensive recipients were characterized by increased peripheral plasma renin activity, lack of change in blood pressure in response to salt loading and restriction, and by increased peripheral and renal resistance. In contrast, on the same protocol in a group of patients with essential hypertension, blood pressure fell significantly on a low-salt intake. Peripheral resistance in hypertensive transplant recipients fell in response to saline loading, in contrast to the effects in normotensive transplant recipients. Hypertensive patients with retained native kidneys as compared to those who had these removed prior to transplant, but were still hypertensive, differed only with regard to reduced renal plasma flow in the former group. These data are consistent with a predominantly renin-dependent hypertension in these renal transplant recipients. When bilateral nephrectomy or repair of graft renal artery stenosis is being considered, response to captopril may offer a means of selection; acute renal failure on captopril suggests functionally significant renal artery stenosis.
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PMID:Mechanisms of posttransplant hypertension. 388 6

We studied renal vein concentrations of prostaglandin E2 (PGE2) and activity of the renin-angiotensin system in 9 normotensive young men (NT), 17 hypertensive patients with unilateral renal artery stenosis (URS), and 26 patients with essential hypertension (EH) of whom 12 had low renin essential hypertension (LRH). The PGE2 concentration, plasma renin activity (PRA), and angiotensin II (A II) were measured in the inferior vena cava and were compared with the mean concentration for both renal veins under basal conditions and without pharmacological interference. The renal vein PGE2 concentrations were higher in NT (p less than 0.01) and URS (p less than 0.05) than in LRH. However, there were no significant differences in A II concentrations between the groups, nor were there any correlations to PGE2 concentrations. The positive correlation between PRA and PGE2 (r = 0.29, p less than 0.02) indicates that PGE2 may contribute to the activation of the renin-angiotensin system or that there may be a common mechanism for stimulation of both hormonal systems. Our results are not compatible with the hypothesis that a reduction of PGE2 production is a specific feature of patients with EH.
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PMID:Renal prostaglandin E2 and the renin-angiotensin system in hypertensive disorders in man. 388 34

The hormonal responses to the stimulus of changing from resting supine to sitting upright for 15 minutes were assessed in 20 patients with hypertension, divided into 2 groups. 8 patients had essential hypertension (EH) and 12 unilateral renal artery stenosis (URS). The prostaglandin E2 (PGE2) concentration, plasma renin activity (PRA), angiotensin II (A-II) concentration, and norepinephrine (NE) concentration were measured in renal vein blood using specific methods. The PGE2 concentration increased after sitting for 15 minutes in all patients (p less than 0.001), but the increment was significant only in those with URS. The PRA was lower both at rest and after sitting up in the EH group than in the URS group. After sitting up the A-II concentration increased more in patients with URS than in those with EH (p less than 0.05). NE levels rose significantly when all patients were included (p less than 0.01), mainly owing to changes in the EH group. Supine and sitting PRA and A-II were correlated (r=0.47 and r=0.52; both p less than 0.05), and also sitting PGE2 and A-II (r=0.46, p less than 0.05). The inverse relation between PGE2 and NE for the difference in hormone concentrations between supine and sitting (r=-0.44, p less than 0.05) may be explained by an inhibitory effect of PGE2 on renal NE release, earlier observed in experiments in vitro. Similar changes in PGE2 and the measured components of the renin-angiotensin system in response to change in posture may indicate these factors are interrelated.
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PMID:Hormonal responses to change in posture in hypertensive man. Evaluation by measurements of prostaglandin E2, renin activity, angiotensin II, and norepinephrine in renal venous blood. 389 17

The putative role of the central nervous system in the maintenance of elevated blood pressure in patients with essential hypertension (EH) and renal hypertension [unilateral renal parenchymal disease (RPD) and unilateral renal artery stenosis (RAS)] was studied by investigating the cardiovascular and hormonal effects of the predominantly centrally acting sympatholytic agent, clonidine. Oral clonidine lowered blood pressure substantially in all three groups. Levels of plasma renin activity were unchanged in EH and RAS but progressively fell in RPD. Plasma noradrenaline levels fell in all three groups. Clonidine therefore reduced blood pressure to the same extent in three distinct groups of hypertensives, in two of which the initiating cause was undoubtedly renal. This indicates that, although the primary cause differed, a prominent factor sustaining hypertension may have been an increase or an inappropriate maintenance of central pressor mechanisms.
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PMID:Cardiovascular and hormonal effects of clonidine in patients with essential hypertension and renal hypertension. 391 57

In a previous study we observed an increase in urinary cyclic AMP in labile hypertension in the upright position and during isoproterenol infusion, in contrast to a decrease in control subjects. In the present study we measured the plasma level of cyclic AMP in control subjects and patients with various types of hypertension. We obtained the following results: (1) plasma cyclic AMP increases in response to upright posture in control subjects and hypertensive patients; (2) values of cyclic AMP in the recumbent and upright positions are comparable in control subjects and patients with essential hypertension, but are significantly higher in those with true renovascular hypertension due to bilateral renal artery stenosis; (3) propranolol inhibits the increase of plasma cyclic AMP in response to posture in control subjects, but has an opposite effect in labile hypertension where there is a further increase; (4) the rise in blood pressure in pheochromocytoma is associated with a considerable increase in plasma cyclic AMP.Present and previous data suggest that kidney handling of cyclic AMP is abnormal in hypertension, and that the specific defect may be related to the type of hypertension.
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PMID:Plasma adenosine 3',5'-cyclic monophosphate in human hypertension. 436 18


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