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

A 32-year old hypertensive woman with bilateral renal artery stenosis of more than 50% on both sides was studied. Renal vein renin levels were low (0.3 ng/ml/h on the right side and 0.42 on the left) before surgical correction of the left renal artery. Thereafter, blood pressure was only temporarily reduced. Four months later a repeat angiography demonstrated a widely patent left renal artery and the stenosis on the right side was unchanged. Renal vein renin was 5.12 on the left and 11.2 on the right. Subsequent operation on the right side lead to normalization of blood pressure. Thus, our patient seems to demonstrate in sequence the characteristics of the tow types of experimental renovacular hypertension known as "one kidney hypertension" and "two kidney hypertension". Our findings usggest that the pathomechanisms of these experimental models are operative in man too.
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PMID:Reversal of "one kidney" to "two kidney" tipe of Goldblatt hypertension in a patient with bilateral artery stenosis. 91 16

In 7 hypertensive patients with renal artery stenosis and in 1 patient with hypertension and unilateral pyelonephritic nephrophthisi the influence of the angiotensin II antagonist, saralasin on systemic hemodynamics was studied. In the patients with normal renin infusion of saralasin produced an increase in total peripheral resistance, in patients with elevated renin a decrease in peripheral resistance was observed. In 3 patients who had extremely high renin levels while under sodium saralasin produced a dangerous drop in blood pressure concomitant with a marked decrease in cardiac output and in central venous pressure, heart rate remained unchanged or increased just slightly. The findings suggest that in patients with high plasma renin peripheral resistance, venous tone, venous retrun, and cardiac output are to a large extent controlled by circulating angiotensin II.
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PMID:[Hemodynamic effects of sar1-ala8-angiotensin in patients with renovascular hypertension (author's transl)]. 91 18

Renal artery stenosis, either fibromuscular or atheromatous, is probably the most common cause of secondary hypertension in man. Both of these diseases are active, ongoing processes that may be ameliorated but not cured by medical or surgical treatment. The clinical history and examination of the patient with hypertension may help differentiate renovascular hypertension from essential hypertension. The presence of a systolic-diastolic or continuous bruit is often an indicator of severe renal artery stenosis. Systemic hypertension is the physiologic consequence of significant renal artery stenosis. Knowledge of the basic concepts of the renin-angiotensin-aldosterone system, as has evolved from experimental models of renovascular hypertension, forms the basis for understanding the process of evaluation and treatment of such patients. The treatment of choice for the patient with severe hypertension and a functionally significant renovascular lesion is surgical--both in terms of successful treatment of hypertension and improved long-term prognosis. Diligent periodic reevaluation of these patients as well as those with less severe hypertension who are receiving medical treatment enables the physician to select the proper management that offers optimal control of patient blood pressure and avoids target-organ damage to the kidneys, central nervous system, or cardiovascular system.
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PMID:Management of the patient with renovascular hypertension. 92 May 87

Plasma renin activity (PRA) was determined in both renal veins of 37 patients with angiographically proven renal artery stenosis. Renal venous PRA was determined in 17 patients without furosemide stimulation and in 20 patients before and 15 and 30 min after intravenous injection of 40 mg furosemide. 21 of 37 patients showed abnormally high peripheral PRA. In the 17 patients in whom renal venous PRA was measured without stimulation, 11 showed a PRA ratio (PRA stenotic side/PRA unaffected side) greater than or equal to 1.5. The 20 patients in whom stimulation with furosemide was performed were divided into 2 groups each containing 10 patients: The first group was characterized by an increase in PRA ratio after furosemide stimulation, while in the second group this PRA ratio decreased. In the first group mean duration of hypertension was 4.5 years compared to 7.5 years in the second group. In 17 of 37 patients renal artery stenosis was corrected by surgery. After operation 12 patients became normotensive and in 2 patients hypertension improved. There was no effect of renovascular surgery on blood pressure in only 3 patients. None of these patients showed an increasing ratio in response to furosemide. Our results suggest that the validity of renal venous PRA measurements is enhanced when the procedure is performed before and after administration of furosemide.
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PMID:[Studies on the differential determination of renin activity in renal venous blood in renal artery stenosis]. 92 40

The frequency of underlying renal or renal artery disease, and the incidence of vascular complications were reviewed in a series of 136 cases of primary hyperaldosteronism. This was in order to investigate the possible existence of 'tertiary' hyperaldosteronism, and to examine the commonly held view that primary hyperaldosteronism is a relatively benign form of hypertension. Ten cases (7-4 per cent) had evidence of renal artery stenosis and eleven (8-1 per cent) parenchymatous renal disease. In comparison with the reported frequency in large general series of hypertensives, these data show no evidence of an excess of underlying renal disease. It is unlikely, therefore, that autonomous aldosterone secreting adenomata occur commonly as a consequence of prolonged secondary hyperaldosteronism. Four cases (2-9 per cent) had evidence of the malignant-phase of hypertension, and over a mean observation time of 5-9 years, 31 cases (22-8 per cent) developed 39 vascular complications. It appears, therefore, that vascular complications are not rare in primary hyperaldosteronism, and early and effective treatment is thus necessary.
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PMID:Renal abnormalities and vascular complications in primary hyperaldosteronism. Evidence on tertiary hyperaldosteronism. 94 42

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

The angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) was given to 27 patients with different forms of secondary hypertension. The blood pressure fell in 6 of 7 patients with renal artery stenosis and in 4 of 10 patients with terminal renal failure on regular hemodialysis. No change or a rise in blood pressure was observed in 3 patients with Cushing's syndrome, 4 patients with primary aldosteronism, 3 patients with hypertension and a unilateral small kidney of other than renovascular origin, and 6 patients with terminal renal failure. It can be concluded from the results that angiotensin II is involved in the pathogenesis of renovascular hypertension and in some cases of hypertension accompanying chronic renal failure.
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PMID:[Effect of the angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) on the blood pressure in secondary hypertension]. 101 96

Renovascular hypertension caused by renal artery stenosis was a coincidental discovery in 5 of the 6 patients presented. They did not have any comlaint and it was by routine bloodpressure measurement that hypertension was diagnosed. In one patient without hypertension stenosis of both renal arteries was seen on the aortography for an infrarenal aortic occlusion. Depending on the extent and localisation of the stenosis unilateral renal artery stenosis was treated by a saphenous vein graft interposition, or by an aortorenal vein patch. In a man with bilateral renal artery stenosis a venous bridge was constructed. Once an unilateral nephrectomy was necessary, the kidney being atrophic and a vascular correction impossible.
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PMID:Renal artery stenosis and occlusion. 101 82

Sar1-Ala8-angiotensin II was infused intravenously (10 mug/kg/min) in 14 patients with renovascular hypertension, including 11 with renal artery stenosis. Brachial artery pressure and heart rate remained unchanged in six patients who were on a daily sodium intake of 130 mEq. In 12 tests performed after sodium depletion, the decrease in mean arterial pressure ranged from 13 to 76 mm Hg and showed a significant correlation with the plasma renin concentration prevailing immediately before the infusion of the drug (r = 0.81; p less than 0.001). The hypotensive response was due to a drop in total peripheral resistance. Heart rate and cardiac output showed slight increases 10 min after the start of saralasin infusion.
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PMID:Haemodynamic effects of Sar1-Ala8-angiotensin II in patients with renovascular hypertension. 101 67

Angiography is the most important diagnostic procedure for evaluation of renovascular hypertension. Technique and limits of this method as well as possible ways of improving its diagnostic value are discussed. The pathogenetic significance of a renal artery stenosis in hypertension and the prognosis for a vascular surgical intervention is discussed in the light of bilateral renin determination and the 138 Xe method of measuring intrarenal hemodynamics.
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PMID:Angiographic aspects of renovascular hypertension. 102 71


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