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

Renin activities were determined in plasma and in single, microdissected juxtaglomerular apparatus in 19 patients with unilateral renal artery stenosis. The mean juxtaglomerular apparatus renin concentration in the stenosed kidneys was 5.5 +/- 1.2 (SEM) mug.l-1.h-1 which is about ten times that of the suppressed renin concentration in the contralateral kidneys (0.6 +/- 0.05 mug.l-1.h-1). On the affected side a positive correlation was found between intrarenal and renal venous renin concentration (r = 0.93; p less than 0.001). Both intrarenal and renal venous renin concentrations of the stenosed kindeys were positively correlated to renin secretion rates, as calculated from renin analysis in plasma from the vena cava and renal veins. No relationship could be demonstrated between intrarenal or renal venous renin concentration and the degree of blood pressure elevation or transstenotic pressure gradient. However, a positive correlation was evident between peripheral plasma renin activity and diastolic blood pressure (r = 0.88; p less than 0.001). Comparative enzyme kinetic analyses of renin from the juxtaglomerular apparatus and renal venous plasma were performed using sheep substrate. The lowest apparent Km-values of renin were found in renal venous plasma from the stenosed kidneys (198 +/- 13 mug/l) compared with the contralateral side (301 +/- 20 mug/l; p less than 0.001). Mean apparent Km-values of juxtaglomerular apparatus renin in the stenosed (270 +/- 36 mug/l) and contralateral (292 +/- 37 mug/l) kidneys did not differ. No significant differences were found between mean apparent Km-values for renin in peripheral plasma of renovascular hypertensive patients and control subjects using either homologous human or heterologous sheep renin substrate. The results suggest that, in addition to the renin concentration other factors are relevant to chronic high blood pressure in renovascular hypertension.
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PMID:Kidney and plasma renin in human renovascular hypertension. 100 43

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113). 2. The P113-induced fall of the blood pressure did correlate with the log PRA (r=0-888, P less than 0-001). This correlation was found irrespective of different types of hypertension and treatment schedules. 3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency. 4. No incication was found that a given PRA is of special importance for blood pressure elevation in different patients. 5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.
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PMID:Change in the renin dependency of blood pressure induced by volume depletion and/or propranolol therapy in hypertensive patients. 107 4

1. The syndrome of malignant hypertension in man and animals has three fundamental components: high blood pressure, activation of the renin-angiotensin system and the rapid development of necrotizing arteriolar disease. 2. The high blood pressure can be associated with different conformations of the arteriolar microcirculation. The emergence of an arteriolar reaction pattern characterized by the formation of focal dilatations, with intervening constricted segments, is of fundamental pathophysiological importance. 3. Activation of the renin system is reflected in an increased renin secretion rate from the kidneys and an increased rate of angiotensin II generation in the pulmonary vascular bed. 4. The crucial pathogenetic process, leading eventually to severe arteriolar wall damage, is a penetration of plasmatic macromolecules into the wall of distended arteriolar segments, as observed in states of severe experimental hypertension. 5. Renin can induce vascular disease, but hypersecretion of renin is not a necessary condition for the development of hypertensive arteriolar necrosis.
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PMID:The renin-angiotensin system and the pathogenesis of vascular disease in malignant hypertension. 107 5

1. In forty-one patients who underwent renal homotransplantation the following measurements were made: (a) blood flow and its distribution in the transplanted kidney as measured by the 85-Kr washout method; (b) renin release in the renal vein of the transplant; (c) arteriovenous difference in plasma renin activity (PRA) of the recipient's remaining left kidney. 2. Eleven transplanted patients were normotensive. Renal haemodynamic data were comparable with those obtained in potential kidney donors. 3. Three hypertensive patients had chronic rejection. The mean renal blood flow and the percentage flow in the first component of the washout curve were reduced. Renin release from the transplant, however, was normal. 4. Ten hypertensive patients had transplant artery stenosis. In eight of them renin release from the grafts as well as peripheral PRA were within normal range. This result is similar to experimental data obtained in Goldblatt renovascular hypertension. The two patients with the tightest artery stenosis had an elevated renin release from the transplant. 5. Thirteen hypertensive patients had elevated arteriovenous difference in PRA of the recipient's own left kidney. Peripheral PRA was significantly higher than in normotensive patients. Left nephrectomy relieved hypertension in ten of them; three have not so far undergone nephrectomy. 6. In four other cases hypertension was also relieved by removal of the patient's own kidney; however, the arteriovenous difference in PRA of that kidney fell within normal range.
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PMID:Permanent hypertension after renal homotransplantation in man. 109 19

Hypertension appeared to be related to stenosis of the hypogastricrenal artery system in 5 patients among 153 recipients of renal allografts. Renin assay and arteriography were crucial in the comprehensive evaluation of patients whose hypertension was not clearly related to rejection or excessive sodium intake. Hypereninemia was persistent in 4 of the 5 patients. Stenoses of the transplant renal arteries in three patients were caused by extensive intimal plaque formation. In one patient, periarterial fibrosis caused reduction of flow; 180 degrees torsion of the anastomosis resulted in stenosis in the fifth patient. Surgical correction is difficult and may be facilitated by a transabdominal approach. Vein bypass is probably preferable to patch angioplasty for intimal lesions. Following operation, hypertension was ameliorated and function improved in all patients. Rejection, which has been suggested as one of the causes of intimal plaque formation, ultimately led to the loss of the transplant in one patient. Function is normal in two patients; two patients have evidence of chronic rejection. No effort should be spared to evaluate this special group of patients whose transplant function can predictably be prolonged by decisive surgical management.
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PMID:Hypertension due to renal artery stenosis in transplanted kidneys. 109 91

Hypertension in endocrine disorders (Cushing's syndrome, Conn's syndrome, Pheochromocytoma) is frequently accompanied by a confusing clinical symptomatology. The underlying pathology is a cortical hyperplasia or a tumor of the adrenal cortex or medulla. The differentiation from other causes of hypertension is primarily based upon laboratory findings (plasma and urinary concentration of cortico-steroids, Renin, Angiotensin and catecholamines as well as their derivates). The preoperative tumor localization by urography, arteriography and adrenal venography as well as the visualization of glandular hypertrophy by adrenal venography is of fundamental importance with regard to treatment of these disorders.
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PMID:[Radiology of suprarenal glands (author's transl)]. 117 39

Renin activity in renal vein plasma and in peripheral plasma was measured in twentytwo hypertensive patients presenting unilateral renal artery stenosis or other unilateral renal abnormalities. A discrepancy between peripheral and renal vein renin levels was noted only in one case. In seven patients the difference between the renal vein renin of the diseased kidney and that of its contralateral mate was very significant. They responded successfully to surgery for hypertension, confirming the predictive value of a renal vein renin ratio greater than 1.5. In all the other patients with less significant differences between the renin levels of the two kidneys surgery was not performed because they benefited from the hypotensive therapy.
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PMID:[Diagnostic and prognostic value of the separated renin in hypertension due to monolateral nephropathy]. 122 37

The authors report on the case of a 7 week-old boy, in whom a renal mass was discovered after general symptoms were observed. Within 48 h, cardiac failure secondary to systemic arterial hypertension occurred, requiring intensive care. After a few days of mechanical ventilation and alternating elevated and low blood pressure, improvement was obtained with captopril and frusemide enabling further investigations to be carried out which lead to the diagnosis of Wilms tumor. During left-sided nephrectomy, elevated renin from the left renal vein was found. The post surgical course was excellent. Several authors have reported on the association between arterial hypertension and nephroblastoma as being the result of hyperreninism due to hilar compression; however severe hypertension was uncommon. Renin activity determination from the tumoral tissue had led to a different interpretation, ie primary hyperreninism: in the case of mesoblastic nephroma, only the non tumoral but compressed tissue contains a large quantity of renin; in the case of nephroblastomas, only the tumoral tissue contains renin. The question now is whether all or only certain nephroblastomas secrete renin.
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PMID:[Cardiac failure by major arterial hypertension secondary to nephroblastoma]. 133 61

We investigated the regional balance of endothelin-1 across the renal and leg vascular bed as well as the hemodynamic effects of exogenously administered endothelin-1 in six healthy men. Net regional endothelin-1 balance was calculated from the respective arteriovenous differences in plasma concentrations and the corresponding plasma flow, the latter being determined by para-aminohippurate or indocyanine-green dye using appropriate catheter techniques. During constant intravenous (i.v.) infusion of endothelin-1 (0.4 pmol/kg/min), a slight increase in diastolic blood pressure (p less than 0.05) and a decrease in heart rate (p less than 0.01) were observed. In contrast, no significant changes in leg hemodynamics were noted. Renal plasma flow decreased by approximately 30%, and renal vascular resistance increased by 50% as compared with the control (placebo) period (p less than 0.01). Renin plasma concentrations did not change substantially during endothelin-1 infusion. During the control (placebo) period, arterial endothelin-1 plasma concentrations averaged 2.1 +/- 1.0 pM. An equilibrated peptide balance across the leg and a slight renal uptake of endothelin-1 was observed. After endothelin-1 infusion, arterial plasma concentrations of the peptide increased to 4.9 +/- 1.3 pM (p less than 0.01), and a net overall renal and limb uptake of endothelin-1 accounted for approximately 9 and 6% of the infused endothelin-1 amount, respectively. Results showed that at systemic endothelin-1 plasma concentrations, comparable to those which occur in a variety of pathologic conditions such as hypertension or cardiogenic shock, besides pulmonary clearance, renal and limb uptake of the peptide may also contribute to the short half-life (t1/2) of endothelin-1 in humans.
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PMID:Regional hemodynamic effects and clearance of endothelin-1 in humans: renal and peripheral tissues may contribute to the overall disposal of the peptide. 137 85

Synthetic sex steroid administration is a major cause of iatrogenic hypertension but little is known of the haemodynamic or metabolic consequences of these steroids. This study examined the short term blood pressure, volume and metabolic consequences of 5 day administration of synthetic androgen to normal men and synthetic oestrogen or progestogen to normal women. Healthy subjects (8 women, 6 men) on a constant diet took part in each of 3 studies. Males received testosterone undecanoate 120 mg/day (n = 6) and females either ethinyloestradiol 0.3 mg/day (n = 5) or norethisterone 15 mg/day (n = 6) for 5 days in the last week of the cycle. Norethisterone increased lying (+7 mmHg) and standing (+8 mmHg) systolic pressure but the other steroids did not alter blood pressure. All 3 treatments increased body weight. There were no consistent changes in plasma electrolytes or glucose with any steroid, and no urinary sodium retention or changes in urine Na:K ratio. Haematocrit fell on ethinyloestradiol but no steroid significantly increased plasma volume (measured as volume of distribution of 125I human serum albumin). Renin substrate and cortisol rose and renin concentration fell on ethinyloestradiol. These studies suggest that the progestogen component may contribute to the blood pressure raising effects of oral contraceptives.
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PMID:Haemodynamic and metabolic effects of short term administration of synthetic sex steroids in humans. 139 77


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