Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The place of captopril (C) testing in the screening for renovascular hypertension is still controversial. Baseline and C-stimulated plasma renin concentrations (PRC) were measured in 113 hypertensives, who where referred for the exclusion of secondary hypertension. In addition intravenous digital subtraction angiography (DSA) and a renal scintigraphy were performed. When renal artery disease was revealed by DSA or renin was stimulated the renal arteries were visualized by direct arteriography (and treated by angioplasty if possible). 86 patients underwent each diagnostic test: 21% had renovascular hypertension. Unilateral renal artery stenosis (n = 10) was detected by the captopril test (cutoff values: baseline greater than 40 microU/ml, after C greater than 180 microU/ml, sensitivity 100%). Bilateral renal artery stenosis (n = 8) was missed when the disease was equally severe on either side (sensitivity 50%). The specificity of C testing was 82%, overall sensitivity (uni- and bilateral disease 78%, prevalence 21%, predictive value of the positive test 0.56, predictive value of the negative test 0.93). With i.v.-DSA the renal arteries were technically evaluable in 91% (82/92) of cases. The sensitivity for the detection of all renal artery stenoses was 79% (uni-lateral 100%, bilateral 40%, specificity 97%). The sensitivity of renal scintigraphy for the detection of unilateral renal artery stenoses was 50%, for the detection of bilateral renal artery stenoses 43%, specificity 81%. The present study demonstrates the usefulness of captopril for the detection of unilateral renal artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Status of the captopril test in the diagnosis of hypertension]. 268 53

Seventy-two patients, aged 6-69 years, were operated on because of presumed renovascular hypertension and subjected to follow-up studies for 4-60 months (mean 28). Unilateral renal artery stenosis was present in 47 patients. Surgery was followed by normalization of blood pressure (BP) in 28 and improvement in 7, whereas 12 showed no response. Sixteen were below the age of 40 and only one failed to respond to surgery. Peripheral venous plasma renin activity (PRA) was increased in 32 and urinary aldosterone elevated in 22 of 35 patients responding favourably to surgery. Renal vein PRA was higher from the kidney with the stenotic renal artery as compared to the contralateral side in all patients responding to surgery. Preoperative peripheral PRA difference was also found in 7 of 12 patients not responding to surgery. Preoperative peripheral PRA was increased in 26 of the patients becoming normotensive after surgery. In 20 of these patients normalization of BP was associated with a fall in peripheral PR. Twenty-five patients had bilateral renal artery stenosis. Four of them had severe hypertension, renal insufficiency and generalized atherosclerosis. They died in immediate connection with operation. Unilateral operation, performed in 11 of the remaining 21 patients, was followed by normalization of BP in 3 and no response in 8. Bilateral reconstructive surgery, performed in 10 patients, resulted in normotension in 2 and improvement in 7. Our studies indicate that determination of peripheral PRA and/or urinary aldosterone can serve as a useful prognostic indicator after surgery in hypertensive patients with renal artery stenosis.
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PMID:Pre- and postoperative studies in 72 hypertensive patients with renal artery stenosis, with special reference to renin activity and aldosterone. 703 32

Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
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PMID:Reversible nephrotic syndrome due to high renin state in renovascular hypertension. 773 87

Computed duplex sonography was used to examine the renal arteries in 36 hypertensive children and adolescents (ages 4-17 years) with arterial hypertension of either renal or non-renal origin. Time-averaged flow velocities, maximum blood flow velocities as well as absolute renal blood flow and renal blood flow per gram kidney weight were measured. Normal flow velocities and normal to elevated renal blood flow volume was found in patients with acute glomerulonephritis and those with signs of chronic glomerulonephritis onset. Patients having advanced stages of chronic glomerulonephritis, on the other hand, were characterized by lower levels of all parameters. Unilateral renal artery stenosis was diagnosed correctly in four patients, although one intra-renal artery stenosis escaped imaging. Scarred kidneys exhibited low-normal or reduced flow velocities and renal blood flow volumes corresponded roughly to kidney size and preservation of normal kidney structure. Hypertension in some patients with normal kidneys showed a tendency to cause higher renal blood flow without consistent acceleration of blood flow velocities. We conclude that duplex sonography is a suitable primary diagnostic tool in measuring blood flow velocities and absolute renal blood flow volume in hypertensive children, thus facilitating the choice of the next diagnostic step.
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PMID:Duplex sonography of renal arteries as a diagnostic tool in hypertensive children. 795 7

The purpose of this study was to evaluate acute and chronic autoregulation of blood flow in the cremaster muscle of one-kidney, one-clip (1K1C) hypertensive rats and to investigate alterations of shear stress during the development of hypertension. Unilateral renal artery stenosis and contralateral nephrectomy were performed in half of the rats and a sham operation was carried out in the other half. Mean blood pressure was significantly increased at 1 (38%) and 4 (34%) weeks in 1K1C rats v age-matched controls. Heart rate was significantly increased 15% at 1 week in 1K1C rats but returned to the control level at 4 weeks. Cremaster arteriolar dimensions were measured in vivo by intravital microscopy. Resting diameter of the first-order arteriole (1A) in 1K1C rats was decreased by 25% (P < .05) at 1 week and by 16% at 4 weeks (ns). Measured by the dual-slit technique, total blood flow to the cremaster muscle in 1K1C rats was reduced by 58% (P < .05) at 1 week but was not significantly different from control at 4 weeks. Wall shear rate calculated in the 1A of 1K1C rats was not significantly different from control at 1 week but was elevated 70% (P < .05) at 4 weeks. Therefore, autoregulation of blood flow in skeletal muscle is impaired and/or overridden in the acute phase of 1K1C hypertension. Shear rate, however, did not deviate from the control level until later, which might be the result of impaired function of the endothelium in chronic hypertension.
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PMID:Altered local regulation of blood flow and shear rate in renal hypertension. 826 41

The prevalence of renovascular disease is estimated to be 3%-5% in pediatric patients with hypertension. The utility of non-invasive imaging tests has not been evaluated in children, and renal arteriography remains the diagnostic test of choice. However, there are no established guidelines for the application of this test and information is not available about the likelihood of detecting an abnormality if an arteriogram is performed in children with hypertension. Therefore, we reviewed the yield of renal arteriography in pediatric patients if the test was performed based on the following two criteria: (1) severe hypertension exceeding the 99th percentile for age and sex or (2) failure to control high blood pressure with one antihypertensive drug. During the period 1983-1998, 28 children (mean age 11.7 years) who satisfied one of the above criteria underwent renal arteriography to investigate hypertension. None of the patients were renal transplant recipients. The average duration of hypertension was 11 months and the peak blood pressure was 168/107 mmHg. The renal arteriogram was abnormal in 12 patients (43%). Unilateral renal artery stenosis was the most-common abnormality. When the patients were divided into two groups - those with an abnormal or normal test result - they did not differ in age, sex, or racial distribution. The peak systolic blood pressure was higher in children with an abnormal renal arteriogram (P<0.05). Among those undergoing the arteriogram on the basis of the first criterion, i.e., severe hypertension, 11 of 23 (48%) studies were abnormal. Five children had an arteriogram based on the second criterion--failure to control the blood pressure with one medication--and in 1 patient (20%) the test was abnormal. We conclude that the prevalence of renovascular disease in a population of hypertensive children subjected to renal arteriography is around 40%. Two clinical criteria--namely severe hypertension or failure to control hypertension effectively with one drug--are useful to guide the application of renal arteriography in children with hypertension.
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PMID:Yield of renal arteriography in the evaluation of pediatric hypertension. 1095 35

Connexins (Cxs) are a family of transmembrane proteins that form gap junctions with unique and redundant biophysical functions. Juxtaglomerular cells express Cx40, which is crucial to the control of renin secretion by blood pressure and angiotensin II, and mice that lack Cx40 have high plasma renin and hypertension. To examine whether normal juxtaglomerular cell function depends on the unique properties of Cx40, we measured renin release in mice where the coding sequence for Cx40 was replaced by that for Cx45, using the knock-in method. We first found that the knock-in strategy indeed resulted in expression of Cx45 but not Cx40 in the juxtaglomerular cells of these mice. The plasma renin concentration of the knock-in mice was similar to that in wild-type mice. The high blood pressure of the Cx40 knockout mice was significantly reduced when Cx45 was knocked into the locus but remained mildly elevated compared to wild-type mice. Blockade of angiotensin II formation by enalapril increased the plasma renin concentration in wild-type and the Cx45 knock-in mice but not in the Cx40 knockout mice. Infusion of angiotensin II into isolated perfused kidneys results in decreased renin release, a phenomenon that was attenuated in the Cx40 knockout mice. However, in the Cx45 knock-in mice, angiotensin II suppressed renin release similar to its effect in wild type mice. Unilateral renal artery stenosis increased the plasma renin concentration and blood pressure in both the wild-type and the Cx45 knock-in mice but not in the Cx40 knockout mice. Since Cx40 can be replaced by Cx45, a connexin with a significantly lower conductivity, we suggest that the regulation of renin release is not dependent on the unique electrical properties of these channel proteins.
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PMID:Substitution of connexin40 with connexin45 prevents hyperreninemia and attenuates hypertension. 1921 2

The renin-angiotensin-aldosterone system and cardiac natriuretic peptides [atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)] are opposing control mechanisms for arterial blood pressure. Accordingly, an inverse relationship between plasma renin concentration (PRC) and ANP exists in most circumstances. However, PRC and ANP levels are both elevated in renovascular hypertension. Because ANP can directly suppress renin release, we used ANP knockout (ANP(-/-)) mice to investigate whether high ANP levels attenuate the increase in PRC in response to renal hypoperfusion, thus buffering renovascular hypertension. ANP(-/-) mice were hypertensive and had reduced PRC compared with that in wild-type ANP(+/+) mice under control conditions. Unilateral renal artery stenosis (2-kidney, 1-clip) for 1 wk induced similar increases in blood pressure and PRC in both genotypes. Unexpectedly, plasma BNP concentrations in ANP(-/-) mice significantly increased in response to two-kidney, one-clip treatment, potentially compensating for the lack of ANP. In fact, in mice lacking guanylyl cyclase A (GC-A(-/-) mice), which is the common receptor for both ANP and BNP, renovascular hypertension was markedly augmented compared with that in wild-type GC-A(+/+) mice. However, the higher blood pressure in GC-A(-/-) mice was not caused by disinhibition of the renin system because PRC and renal renin synthesis were significantly lower in GC-A(-/-) mice than in GC-A(+/+) mice. Thus, natriuretic peptides buffer renal vascular hypertension via renin-independent effects, such as vasorelaxation. The latter possibility is supported by experiments in isolated perfused mouse kidneys, in which physiological concentrations of ANP and BNP elicited renal vasodilatation and attenuated renal vasoconstriction in response to angiotensin II.
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PMID:Natriuretic peptides buffer renin-dependent hypertension. 2471 31