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 present study was designed: (a) to examine the contribution of the renin-angiotensin system (RAS) to elevated regional vascular resistance during the onset of aortic coarctation hypertension, and (b) to determine the role of angiotensin II (Ang II)-neural interactions during the maintenance of high arterial pressure (AP). In the first study, rats were instrumented chronically with miniaturized pulsed Doppler flow probes on the right renal and superior mesenteric arteries 3 days prior to complete aortic ligation. After ligation, AP and renal and mesenteric vascular resistances increased significantly. In sham-ligated rats, small increases in AP and decreases in regional vascular resistances were observed. Captopril, administered 6 h postligation, reduced AP and regional vascular resistance in ligated rats to preligation levels, indicating that the RAS was responsible for these acute increases. In the second study, Ang II-neural interactions were examined by treating 12- to 14-day postligation hypertensive rats with captopril or with hexamethonium, a ganglionic blocker, followed by captopril. Depressor responses to captopril were also examined in aortic-ligated rats pretreated with hydralazine. Captopril alone and captopril after hydralazine caused similar reductions in AP (-26 +/- 2% and -27 +/- 1%, respectively). After ganglionic blockade, the depressor responses to captopril were attenuated (-13 +/- 2%). The marked differences in the efficacy of captopril to lower AP in the ganglionic-blocked group of rats suggested that the pressor actions of Ang II were mediated, in part, through indirect actions on the sympathetic nervous system.
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PMID:Hemodynamic, neural, and humoral mechanisms of aortic coarctation hypertension in the rat. 242 87

Captopril has not yet been included in the list of drugs causing hypersensitivity lung disease. We report a patient with hypertension, congestive heart failure, and chronic renal failure who, when rechallenged with captopril, developed upper lung field infiltrates associated with productive cough and striking peripheral eosinophilia. Gallium scan, transbronchial biopsy histologic findings, and direct immunofluorescent study were consistent with an immune-complex-mediated hypersensitivity reaction. There was no other etiology discovered for the patient's eosinophilia, nor was there evidence for an infectious etiology to explain his presentation.
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PMID:Captopril-induced hypersensitivity lung disease. An immune-complex-mediated phenomenon. 252 35

Rats with one kidney clamped (2K1C), both kidneys clamped (2K2C), unilaterally nephrectomized with remaining kidney clamped (1K1C), and normals, were studied using 99mTc mercaptoacetyltriglycine ([ 99mTc]MAG-3) and 131I orthoiodohippurate ([131I]OIH). Clearances of [99mTc]MAG-3 and [131I]OIH were performed after constricted rats became hypertensive. Clearances were repeated after i.v. Captopril. Clearances of [99mTc]MAG-3 and [131I]OIH in normals didn't change significantly after Captopril. Clearances of [99mTc]MAG-3 and [131I]OIH decreased insignificantly after Captopril in the 2K2C model. in the 2K1C group, normal kidney clearance increased ([99mTc]MAG-3 p less than 0.01 and [131I]OIH p less than 0.025) and clamped kidney clearance decreased after inhibition ([99mTc]MAG-3, p less than 0.01, [131I]OIH p less than 0.02). Clearances increased in the 1K1C group after Captopril ([99mTc]MAG-3 p less than 0.0025 and [131I]OIH, p less than 0.001). The ratio of [99mTc]MAG-3 to [131I]OIH before Captopril was 0.81 and 0.84 after Captopril. Changes in renal function after Captopril depend on the model of renovascular hypertension and possibly the dose administered. Technetium-99m MAG-3 clearance parallels [131I]orthoiodohippurate in renovascular hypertension.
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PMID:Technetium-99m MAG-3 clearances after captopril in experimental renovascular hypertension. 252 59

Captopril is commonly prescribed to patients with hypertension and congestive heart failure. Adverse dermatological reactions have been reported in about ten percent of patients receiving captopril. This case report describes a 77-year-old white woman who developed bullous pemphigoid associated with the use of captopril. The patient presented with bullous eruptions localized on the palms of both hands about 50 days after captopril 25 mg bid was started. Biopsy report was consistent with bullous pemphigoid. Captopril therapy was discontinued and the lesions healed after oral corticosteroid therapy was initiated.
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PMID:Bullous pemphigoid associated with captopril. 252 30

This study was initiated to test the hypothesis that attenuation of long-term hypertension with or without regression of left ventricular hypertrophy (LVH) will lower minimal coronary vascular resistance (MCVR). Six-month-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with captopril or hydralazine for a period of 3 mo. Myocardial perfusion, measured with microspheres, and hemodynamic data were obtained in awake, unrestrained rats aged 9 mo. MCVR was calculated from the quotient of mean/myocardial perfusion. Both drugs significantly lowered arterial systolic pressure in both strains of rats, but only captopril was effective in reducing heart mass. Left ventricular MCVR per 100 g was lower in captopril-treated WKY (0.064 +/- 0.012) and SHR (0.079 +/- 0.006) than the untreated controls (SHR: 0.124 +/- 0.006; WKY: 0.098 +/- 0.009), whereas total LV MCVR was unaltered by treatment. Hydralazine tended to lower LV MCVR per 100 g in both strains despite its tendency to increase ventricular mass. Captopril, but not hydralazine, treatment was associated with a significant increase in capillary density in both WKY and SHR. We conclude that the improvement in MCVR is related to both the regression of LVH and to the consequences of lowering arterial systolic pressure. In contrast, the increase in capillary density appears to be related to the decrease in ventricular mass after captopril treatment.
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PMID:Role of lowering arterial pressure on maximal coronary flow with and without regression of cardiac hypertrophy. 2773 36

Two different methods to assess the change of split renal function following angioplasty or bypass grafting were studied in a total of 12 patients with renovascular hypertension. The studies were performed before and within seven days after the therapeutic intervention. Split effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) after injections of I-131 hippuran and Tc-99m DTPA were measured using kidney counting corrected for depth and dose, described by Schlegel and Gates. In six of 10 patients with unilateral renal artery stenosis and in two patients with bilateral renal artery stenoses (two of 4 affected kidneys), the split renal function was improved after the therapeutic intervention, in accordance with the drop in blood pressure and the reduction of plasma renin activity. The improvement in ERPF and GFR was more likely in the patients without severely reduced renal function. In such patients, the improvement in ERPF was more pronounced than that in GFR. And in two patients with functional improvement, the Captopril-induced reduction of split GFR in the affected kidney was disappeared after the intervention. Moreover, in the long-term follow-up of three patients with functional improvement, one patient showed the deterioration of split renal function suggesting the relapse of renal artery stenosis. These results suggest that the combined studies of split ERPF and GFR determinations can be useful to evaluate the therapeutic effect as well as the presence or absence of functional improvement after the intervention.
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PMID:[Assessment of split renal function before and after angioplasty or bypass grafting in the patients with renovascular hypertension]. 253 Mar 76

1. We have investigated the effects of the non-renin-mediated actions of angiotensin converting enzyme inhibitors on the progression of chronic renal failure accelerated by hypertension. For this purpose, we studied the effects of captopril (a thiol-containing angiotensin converting enzyme inhibitor), enalapril (an angiotensin converting enzyme inhibitor without a thiol group) and cysteine (a thiol-containing amino acid which has no angiotensin converting enzyme-inhibitory action) in adriamycin-treated rats with deoxycorticosterone acetate-salt hypertension, in which the renin-angiotensin system was suppressed. 2. There were no significant differences in blood pressure between these groups and the control group [adriamycin-treated group with deoxycorticosterone acetate-salt loading, 206 +/- 7 mmHg (27.4 +/- 0.9 kPa) at week 10]. 3. Massive proteinuria occurred in all groups. At the end of the experiment (at week 10), urinary protein excretion was significantly reduced in the captopril and cysteine groups compared with the control group. No manifest improvements appeared in the enalapril group. 4. Levels of serum creatinine and blood urea nitrogen increased progressively. At week 10, the increases in the serum levels of creatinine were less in the captopril (87 +/- 16 mmol/l) and cysteine (80 +/- 19 mmol/l) groups than in the control group (124 +/- 27 mmol/l) (P less than 0.01). No marked differences were found between the control and enalapril groups. 5. Captopril and cysteine caused more than a three-fold reduction in the focal glomerulosclerosis score when compared with that in the control group, but enalapril did not decrease the score. The extent of tubulointerstitial change was parallel with the focal glomerulosclerosis score. 6. We conclude that the thiol group is possibly involved in the mechanism of the beneficial effects of some angiotensin converting enzyme inhibitors on the progression of chronic renal failure exacerbated by hypertension.
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PMID:Differences in the effects of angiotensin converting enzyme inhibitors with or without a thiol group in chronic renal failure in rats. 254 Sep 31

Patients with severe hypertension and/or congestive heart failure (n = 281) who were unresponsive to other therapies and intolerant to captopril received enalapril treatment (mean dose 19.5 mg/day) under study conditions as part of a Compassionate Use Program. Many of these patients had serious concurrent disorders known to predispose them to a greater risk of adverse experiences and death. The mean duration of enalapril treatment was 29 weeks, with a range of 1 day to approximately 3.5 years. Enalapril was generally well tolerated, and the estimated long term probability of patients terminating enalapril therapy because of adverse effects was low. 20 patients had discontinued captopril treatment because of low white blood cell counts; during subsequent enalapril treatment these reactions resolved in 14 patients, persisted in 2 patients, and could not be evaluated in 4 patients. Captopril-related proteinuria improved or resolved in 9 and persisted in 2 of 15 patients, taste disturbances resolved in 35 and persisted in 2 of 38 patients; and rash resolved in all but 7 of 178 patients during enalapril treatment. 18 patients (6%) discontinued enalapril treatment because of lack of efficacy; 6 of these 18 patients died due to a progression of heart failure, and another 11 patients died for other reasons. The deaths were considered unrelated to therapy with enalapril. Adverse reactions were the reason for discontinuation of enalapril treatment in 53 patients (19%). The most common adverse experiences that resulted in discontinuation of enalapril were: impairment of renal function (5%), hypotension (2%) and rash (2%). No neutropenia, proteinuria, or new taste disturbances were recorded as reasons for discontinuation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerability of long term therapy with enalapril maleate in patients resistant to other therapies and intolerant to captopril. 254 10

MK-0521 and captopril were orally administered to acute (6 to 8 days after unilateral renal artery constriction) and chronic (2 to 2.5 months after the constriction) 2-kidney Goldblatt hypertensive dogs for 7 to 21 days. MK-0521 lowered the blood pressure to similar extents in the acute and chronic stages of hypertension. The antihypertensive effect of MK-0521 was dose-dependent and persistent even after its cessation. Captopril also produced an antihypertensive effect, although the effect in the chronic stage of hypertension was less prominent than that in the acute stage of hypertension. MK-0521 was more inhibitory on the renin-angiotensin system than captopril. In the acute stage of hypertension, the dogs treated with MK-0521 had increased angiotensin converting enzyme (ACE) activity, while they had decreased plasma angiotensin II level and elevated plasma angiotensin I level and plasma renin activity. These results clarified the inhibitory effect of MK-0521 on ACE. In contrast, in the chronic stage of hypertension, MK-0521 showed no depression of plasma angiotensin II. There were no significant changes in daily urinary volume, and renal clearances of sodium, potassium and creatinine. These results suggest that the major mechanism of the antihypertensive effect of MK-0521 in 2-kidney Goldblatt hypertensive dogs is an inhibition of the ACE. In addition, the different effects in the acute and chronic hypertensive dogs suggest that some differences exist in the mechanisms of maintaining blood pressure between the two stages of 2-kidney Goldblatt hypertensive dogs.
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PMID:[Antihypertensive effect of repeated oral administration of MK-0521 in 2-kidney Goldblatt hypertensive dogs]. 254 80

The activity of converting enzyme was determined in 19 patients with Cushing's disease using Friedland and Silverstein technique. Statistically significant increase in the activity of this enzyme was noted in the majority of the examined patients in comparison with healthy subjects. Therefore, inhibitors of the converting enzyme (Captopril) are justified in the treatment of the arterial blood hypertension in Cushing's disease.
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PMID:[Activity of angiotensin converting enzyme (ACE) in cushing's disease]. 255 63


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