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

Captopril-stimulated renography is emerging as a useful diagnostic tool for the evaluation of the hypertensive patient suspected of having renovascular hypertension (RVHT). This overview focuses upon the alterations in renal hemodynamics and function induced by renal artery stenosis (RAS) and reviews the effects of angiotensin-converting enzyme (ACE) inhibition upon blood pressure and kidney function in the various experimental models of RVHT. Understanding the effects of ACE inhibition upon the kidney distal to a stenosis and appreciating the potential effect of sodium balance or antihypertensive medications are crucial in anticipating the putative changes in the radionuclide studies of the renovascular bed following ACE inhibition.
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PMID:Renal physiology of renal artery stenosis. Implications for captopril-stimulated renography. 177 81

Captopril renography is an excellent technique for investigating renovascular hypertension and other renal disturbances. However, many variables affect the usefulness of renographic data. The choices of radiopharmaceutical, converting enzyme inhibitor, and the type of imaging done must be made with care. Additionally, the method for selecting a study population must be carefully examined. Incorrect choices can render a study's data valueless. In this paper we delineate the questions that need to be considered before undertaking a renographic study.
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PMID:Captopril renography. Considerations in the selection of radiopharmaceuticals, provocative agents, and hypertensive subjects. 177 82

Captopril radionuclide test (CRT) has been introduced in clinical practice as a screening test for renovascular hypertension, since it allows the detection of the decrease of glomerular filtration rate that may be induced by angiotensin converting enzyme inhibition (25 mg oral captopril) in kidneys ipsilateral to a renal artery stenosis. However, due to the low prevalence of the disease, experiences in single centers may hardly satisfy the need for representative series of patients to validate the test. Nineteen centers participated in a collaborative study (CRT European Multicenter Study) that collected data from 424 patients. Here we report on the first results obtained by inspective renographic analysis. The captopril radionuclide test greatly potentiated the diagnostic performance of conventional renography and the accuracy was maximal when relying simply on postcaptopril findings alone. Specificity was 84.1% in the overall population and 91.8% in uncomplicated patients without nephropathy and renal insufficiency. Taking into account the sole arteriographic diagnosis, sensitivity was 73.2% or 90.7% for the subjects with unilateral or bilateral stenosis and an angiographic degree of stenosis greater than or equal to 70%. On the other hand, when a successful outcome of blood pressure after revascularization or nephrectomy was considered as the gold standard for the diagnosis of renovascular hypertension, a high sensitivity was obtained (92.7%). Moreover, the test became negative after intervention in the great majority (88%) of patients who had a positive preintervention CRT and a normalization of blood pressure after revascularization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:European Captopril Radionuclide Test Multicenter Study. Preliminary results. Inspective renographic analysis. The European Captopril Radionuclide Test Multicenter Study Group. 177 83

Lipid peroxides and fluorescent serum proteins, possible markers of free radical activity, are increased in diabetic patients, particularly those with angiopathy. Captopril, an angiotensin converting enzyme (ACE) inhibitor, scavenges free radicals in vitro independently of ACE inhibition. This is probably due to the presence of a sulphydryl group which is not present in other ACE inhibitor drugs. We have compared the effects of captopril and enalapril on free radical activity in thirty-two diabetic subjects with hypertension (BP greater than 160/95 mmHg). After a three week run-in period on no antihypertensive therapy, patients were randomly allocated to receive captopril or enalapril, the dose titrated according to BP response. After three months, BP was well controlled in both groups and glycaemic control unchanged. Both drugs were associated with a reduction of fluorescent IgG (captopril:Baseline [BL] 0.564 vs. 12 weeks [w] 0.428, P less than 0.05, enalapril:BL 0.603 vs. 12w 0.422 P less than 0.05) and thiobarbituric acid reactive material (captopril:BL 2.35 nmol MDA vs. 12w 1.46 nmol, P less than 0.05, enalapril:BL 2.44 nmol vs. 12w 1.72 nmol, P less than 0.01). In contrast to in vitro studies, there was no significant difference between the drugs when used in therapeutic doses, questioning a hypothesised advantage of captopril over enalapril.
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PMID:Comparison of the free radical scavenging activity of captopril versus enalapril: a three month in vivo study in hypertensive diabetic patients. 179 11

In an attempt to evaluate the influence of hypertension and antihypertensive agents on IgAN, IgAN and hypertension experimental models were induced in SD rats and divided into 4 groups: (1) IgAN(n = 8); (2) IgAN+by hypertension(n = 8); (3) captopril 4mg/100gBW/d, for 42 days administered to rats as group (2) (n = 8); (4) nifedipine 300ug/100gBW/d, for 42 days administered to rats as group (2) (n = 8). Blood pressure was measured at the 12th, 14th, 16th, 18th and 20th week. Urinary protein, serum angiotensin II (AT II) and renal pathologic changes were examined at the 20th week. Our results suggest that hypertension worsens IgAN by glomerular mesangial proliferation in early stages. Though Captopril has the same therapeutic effect on hypertension as Nifedipine does, the former has been proven to have potentially beneficial effects on diminishing proteinuria as well as mesangial lesions. This is consistent with the suppression of serum ATII which favours glomerular microcirculation.
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PMID:[The influence of hypertension and antihypertensive agents on experimental IgA nephropathy (IgAN)]. 180 38

Renal artery stenosis (RAS) is a rare cause of hypertension. Radiological tests can disclose the morphological changes, but not their functional effect on renal function and perfusion. Normalization of the blood pressure can be achieved by intervention (operation, percutaneous transluminal renal angiography; PTRA), in cases of prolonged RAS-induced hypertension long-term preservation of the organ function is most important. The purpose of this study was the validation of captopril renography as a screening test for hypertension secondary to RAS prior to PTRA. Captopril renography with 99mTc-MAG 3 has a high sensitivity (94%) and acceptable specificity (88%) for the screening of hypertensive patients. The positive predictive value is 74% and the negative predictive value 98%, compared with the "gold standard" of angiography.
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PMID:[Captopril-renal function scintigraphy in the clarification of arterial hypertension]. 182 97

The goal of the present study was to compare the effects of cilazapril, a new long-acting angiotensin converting enzyme inhibitor, to those of captopril and hydralazine on the coronary vascular bed. For this purpose, spontaneously hypertensive rats were treated for 4 months with either placebo, 10 mg/kg/day cilazapril, 100 mg/kg/day captopril, or 10 mg/kg/day hydralazine. At the end of treatment, maximal coronary blood flow was measured during maximal coronary vasodilation with adenosine in isolated perfused hearts. Cilazapril was the most effective drug in increasing maximal coronary blood flow. Captopril was less effective in improving maximal coronary blood flow but was as effective as cilazapril in reducing cardiac hypertrophy. Hydralazine had an extremely small effect on cardiac hypertrophy and maximal coronary flow reserve. The ranking of efficacy was similar for the reduction of vessel wall hypertrophy in the coronary arteries and arterioles. Because of the higher efficacy of cilazapril compared with captopril, a second experiment was performed in which 10 mg/kg/day cilazapril was compared with 100 mg/kg/day captopril and 300 mg/kg/day captopril after 1 month of treatment. Captopril increased maximal coronary flow and decreased cardiac hypertrophy to the same level as cilazapril only at the highest dose. We conclude that angiotensin converting enzyme inhibitors, in contrast to hydralazine, can increase markedly maximal coronary flow in spontaneously hypertensive rats but that this increase does not always parallel the decrease of cardiac hypertrophy and is closely dose dependent.
Hypertension 1991 Oct
PMID:Effects of two angiotensin converting enzyme inhibitors and hydralazine on coronary circulation in hypertensive rats. 183 28

Although the role of angiotensin II (Ang II) in the pathogenesis and progression of the failing heart is uncertain, previous reports have suggested that myocyte injury may be a component in this process. In this study, we investigated this possibility in more detail. Cardiotoxic effects of nonacutely hypertensive doses of Ang II were examined in 90 rats, including those receiving an angiotensin infusion (200 ng/min i.p.) and those with renovascular hypertension, where endogenous stimulation of Ang II occurred. Myocyte injury and wound healing resulting from these treatments were evaluated by 1) immunofluorescence after in vivo monoclonal antibody labeling of myosin to detect abnormal sarcolemmal permeability, 2) [3H]thymidine incorporation into DNA, to detect fibroblast proliferation, and 3) light microscopic evidence of myocytolysis and subsequent scar formation. We found that exogenous Ang II produced multifocal antimyosin labeling of cardiac myocytes and myocytolysis, which were maximal on days 1-2 of the infusion. Subsequently, DNA synthesis rates were increased, with fibroblast proliferation reaching peak levels on day 2 (Ang II-treated rats, 90.0 +/- 18.6 cpm/micrograms DNA; control rats, 11.4 +/- 2.3 cpm/micrograms DNA; p less than 0.05); microscopic scarring was found on day 14 and represented 0.12 +/- 0.02% of the myocardium. Concurrent treatment with both propranolol (30 mg/kg/day s.c.) and phenoxybenzamine (5 mg/kg/day i.m.) did not attenuate Ang II-induced antimyosin labeling. Increased endogenous Ang II, resulting from renal ischemia after abdominal aortic constriction, produced both antimyosin labeling and increased rates of DNA synthesis like that observed with Ang II infusion. Both myocyte injury and fibroplasia were prevented with captopril (65 mg/day p.o.), but this protective effect was not seen with reserpine pretreatment. Infrarenal aortic banding without renal ischemia, on the other hand, produced hypertension without necrosis. We conclude that pathophysiological levels of endogenous as well as low-dose exogenous Ang II were associated with altered sarcolemmal permeability and myocytolysis with subsequent fibroblast proliferation and scar formation. Myocyte injury was unrelated to the hypertensive or enhanced adrenergic effects of Ang II or to hypertension per se. Captopril was effective in preventing myocyte injury in renovascular hypertension. The mechanism(s) responsible for Ang II-induced necrosis will require further study.
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PMID:Cardiac myocyte necrosis induced by angiotensin II. 183 62

It is well known that angiotensin antagonists cause increase of renal blood flow. We have examined, using duplex Doppler sonography, the changes of renal blood flow velocity induced by oral administration of 50 mg. of Captopril. We examined 19 kidneys in 17 subjects without hypertension. Both peak systolic and diastolic velocities were measured at renal hilum and at arcuate arteries, and the resistive index (RI) was calculated. In conclusion duplex Doppler sonography shows significant increase of blood flow velocities both at the hilum and at the arcuate arteries, without variation of the RI, thus showing that changes affect the whole Doppler wave, both in systole and diastole.
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PMID:[Captopril-induced changes in renal flow: evaluation using Doppler echography]. 183 67

To enhance diagnosis and predict improvement in blood pressure control following surgery or renal angioplasty in patients with hypertension and renal artery stenosis (RAS), we employed captopril renography in 113 clinically selected patients, all of whom had renal angiography to verify the diagnosis. Criteria for normal captopril renograms were established from an initial cohort of 23 hypertensive patients with normal angiograms who had been judged to be at high risk for RAS using the same clinical criteria. Renal revascularization or nephrectomy was performed in 45 patients and the success of the procedure was determined in the 40 patients for whom 3-month follow-up was available. In these 113 patients, 58 (51%) had RAS. Captopril renography was 91% sensitive and 87% specific in identifying or excluding RAS. Diagnostic utility was preserved in those patients with renal insufficiency (serum creatinine equal to or greater than 1.5 mg/dL) (n = 46). Scintigraphic abnormalities induced by captopril were strongly associated with cure or improvement in blood pressure control following revascularization or nephrectomy (16 of 19), while the lack of captopril-induced change was associated with failure of such intervention (17 of 21) (P = .0001). We conclude that captopril renography is sensitive and specific for the diagnosis of RAS in a clinically selected high-risk group of hypertensives, and that the test accurately predicts the success or failure of therapeutic intervention.
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PMID:Captopril renography in the diagnosis of renal artery stenosis and the prediction of improvement with revascularization. The Yale Vascular Center experience. 183 92


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