Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new captopril research articles will be listed here shortly after becoming available to us.
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Medical research on captopril
Congenital nephrotic syndrome of the finnish type.
Ghana Med J. 2008 Mar; 42(1): 42-4
Badoe E, Kumoji R
SummaryCongenital Nephrotic Syndrome of the Finish type (CNF) is a rare and severe disease. A neonate with CNF is described. The diagnosis carries a dramatically poorer prognosis than nephrotic syndrome diagnosed after one year. The clinical course is one of persistent oedema and recurrent infections leading to death. The gene for the Finish type has been mapped to the long arm of chromosome 19. Case reports show it to be responsive to captopril and indomethacin. It is uniformly resistant to steroids and immunosuppressive drugs.
Renal and Hormonal Responses to Direct Renin Inhibition With Aliskiren in Healthy Humans.
Circulation. 2008 Jun 16;
Fisher ND, Danser AH, Nussberger J, Dole WP, Hollenberg NK
BACKGROUND: -Pharmacological interruption of the renin-angiotensin system focuses on optimization of blockade. As a measure of intrarenal renin activity, we have examined renal plasma flow (RPF) responses in a standardized protocol. Compared with responses with angiotensin-converting enzyme inhibition (rise in RPF approximately 95 mL . min(-1) . 1.73 m(-2)), greater renal vasodilation with angiotensin receptor blockers ( approximately 145 mL . min(-1) . 1.73 m(-2)) suggested more effective blockade. We predicted that blockade with the direct oral renin inhibitor aliskiren would produce renal vascular responses exceeding those induced by angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Methods and Results-Twenty healthy normotensive subjects were studied on a low-sodium (10 mmol/d) diet, receiving separate escalating doses of aliskiren. Six additional subjects received captopril 25 mg as a low-sodium comparison and also received aliskiren on a high-sodium (200 mmol/d) diet. RPF was measured by clearance of para-aminohippurate. Aliskiren induced a remarkable dose-related renal vasodilation in low-sodium balance. The RPF response was maximal at the 600-mg dose (197+/-27 mL . min(-1) . 1.73 m(-2)) and exceeded responses to captopril (92+/-20 mL . min(-1) . 1.73 m(-2); P
J Physiol. 2008 Jun 12;
De Gobbi JI, Menani JV, Beltz TG, Johnson RF, Thunhorst RL, Johnson AK
The inflation of an intravascular balloon positioned at the superior vena cava and right atrial junction (SVC-RAJ) reduces sodium or water intake induced by various experimental procedures (e.g., sodium depletion; hypovolemia). In the present study we investigated if the stretch induced by a balloon at this site inhibits a rapid onset salt appetite, and if this procedure modifies the pattern of immunohistochemical labeling for Fos protein (Fos-ir) in the brain. Male Sprague-Dawley rats with SVC-RAJ balloons received a combined treatment of furosemide (Furo - 10 mg/kg bw) plus a low dose of the angiotensin-converting enzyme inhibitor captopril (Cap - 5 mg/kg bw). Balloon inflation greatly decreased the intake of 0.3 M NaCl for as long as the balloon was inflated. Balloon inflation over a 3 h period following Furo/Cap treatment decreased Fos-ir in the organum vasculosum of the lamina terminalis and the subfornical organ and increased Fos-ir in the lateral parabrachial nucleus and caudal ventrolateral medulla. The effect of balloon inflation was specific for sodium intake because it did not affect the drinking of diluted sweetened condensed milk. Balloon inflation and deflation also did not acutely change mean arterial pressure. These results suggest that activity in the forebrain circumventricular organs and in hindbrain putative body fluid/cardiovascular regulatory regions is affected by loading low pressure mechanoreceptors at the SVC-RAJ, a manipulation that also attenuates salt appetite.
[How urgent is it to decrease high blood pressure?]
Praxis (Bern 1994). 2008 Apr 16; 97(8): 431-6
Ardigo S, Rutschmann O, Waeber B, Pechère-Bertschi A
Severe hypertension represents a frequent problem for the general practitioner. One has to decide if the blood pressure needs to be decreased immediately (hypertensive emergency), or if the blood pressure maybe progressively decreased in a few hours and normalized in a few days (hypertensive crisis). Thus it is crucial to identify on the basis of the clinical history and a careful physical examination, the patients for whom the arterial blood pressure elevation represents an acute danger for organ damage or a vital threat in the absence of immediate blood pressure control. In the case of hypertensive crisis, oral medication is usually sufficient (slow release or GITS nifedipine, nitroglycerin, labetalol, captopril). The hypertensive emergency sometimes requires an oral medication before the admission to the emergency room, then followed by intravenous drug administration (sodium nitroprussiate, nitroglycerin, labetalol).
Angiotensinogen genotype predicts abnormal renal hemodynamics in young hypertensive patients.
J Hypertens. 2008 Jul; 26(7): 1353-1359
Patel TV, Williams GH, Fisher ND
OBJECTIVE: In essential hypertensive patients, blunted renal plasma flow responsiveness to angiotensin II suggests a pathologic increase in angiotensin II in the kidneys. This blunting has been associated with the angiotensinogen 235TT genotype. As several measures of renal function decline with age, we sought to determine the interaction of age and genotype on this intermediate phenotype. DESIGN AND METHODS: Three hundred fifteen participants had renal plasma flow response to subpressor doses of angiotensin II (3 ng/kg/min) measured by para-aminohippuric acid clearance in high-sodium balance. Individuals were divided by median age into young (/=45 years) sets. A subset of participants was also studied after administration of captopril. RESULTS: Age, baseline renal plasma flow, BMI and angiotensinogen 235 genotype independently predicted renal plasma flow responsiveness to angiotensin II. Renal plasma flow responses were lower in older individuals than younger (P = 0.03, hypertensive patients; P = 0.004, normotensive individuals). Both hypertensive patients and normotensive individuals carrying either angiotensinogen 235MM or MT genotypes showed this inverse association (P = 0.005, hypertensive patients; P = 0.05, normotensive individuals). However, among angiotensinogen 235TT homozygotes the pattern differed: normotensive individuals had a fall in renal vascular responsiveness with age (P = 0.01) but hypertensive patients did not (P = 0.72). Young hypertensive patients already showed blunted responses. Of all genotype subsets, only angiotensinogen 235TT hypertensive patients showed enhancement (P = 0.03) of the renal vascular responsiveness to angiotensin II after captopril. CONCLUSION: The angiotensinogen 235TT variant predicts premature blunting of renal vascular responsiveness among young hypertensive patients. This abnormal response is corrected by angiotensin-converting enzyme inhibition. This first report of age and genotype interaction may have important implications in the profiling and management of essential hypertension.
Role of prorenin in the pathogenesis of retinal neovascularization.
Hokkaido Igaku Zasshi. 2008 May; 83(3): 159-65
Yokota H, Takamiya A, Nagaoka T, Hikichi T, Ishida Y, Suzuki F, Yoshida A
PURPOSE: To determine the role of prorenin in the pathogenesis of retinal neovascularization, we evaluated the inhibitory effect of the handle region peptide (HRP) on retinal neovascularization. METHODS: Neonatal C57BL6 mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and placed in room air. The animals received HRP (1.0 or 0.1 mg/kg/day), captopril (10 mg/kg/day), or normal saline from P12 to P17. Following enucleation of the eyes, the retina was dissected for whole-mount retinal sections and semiquantitative analysis of mRNA of vascular endothelial growth factor (VEGF), placental growth factor (PIGF), fms-like tyrosine kinase 1 (Flt-1), fetal liver kinase 1 (Flk-1), angiopoietin 2 (Ang2), and tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2 (Tie2). RESULTS: The average numbers of neovascular nuclei in retinopathy of prematurity treated with normal saline, captopril, and HRP (0.1 or 1.0 mg/kg/day) were 37.2+/-8.6, 7.7+/-3.4, 39.5+/-7.3, and 6.5+/-2.7, respectively. HRP (1.0 mg/kg/day) and captopril inhibited neovascularization in rhodamine-perfused retina; HRP (0.1 mg/kg/day) did not. Semiquantitative analysis of mRNA for angiogenic factors showed that HRP (1.0 mg/kg/day) inhibited overexpression of PIGF, Flt-1, and Ang2. CONCLUSIONS: HRP inhibits retinal neovascularization by interfering with nonproteolytic activation of prorenin, indicating that prorenin may promote retinal neovascularization.
Cancer Gene Ther. 2008 Jun 6;
Solly F, Fish R, Simard B, Bolle N, Kruithof E, Polack B, Pernod G
Tissue-type plasminogen activator (tPA) plays a major role in the fibrinolytic system. According to several reports, tPA may also have antiangiogenic properties, especially in combination with a free sulfhydryl donor (FSD). In the rat C6 glioma model, in vitro and in vivo tPA synthesis by glioma cells is enhanced by differentiation therapy. To address the antiangiogenic potential of tPA in this model, tPA was overexpressed in glioma tumors by ex vivo transduction of C6 cells with a lentiviral vector encoding tPA. The transduced cells were subcutaneously implanted into nude mice. Gene transfer allowed for efficient synthesis of tPA by the C6 tumors. Although the treatment of tPA(+) tumor-bearing animals with the FSD captopril generated angiostatin in situ and reduced endothelial vascularization of the tumors, it had no effect on tumor growth. Alternative mechanisms could account for this lack of effect and consequently have important implications for vascular the treatment of glioblastoma.Cancer Gene Therapy advance online publication, 6 June 2008; doi:10.1038/cgt.2008.36.
[Patient with hypertension and bilateral renal artery stenosis]
Ugeskr Laeger. 2008 Jun 2; 170(23): 2039
Burchardt L, Abrahamsen J
A patient story regarding a young man with hypertension and bilateral renal artery stenosis is presented. The value of renography/captopril renography in connection with selective renal vein renin sampling is discussed.
J Int Med Res. 2008 May-Jun; 36(3): 537-43
Qian YJ, Xiao XJ, Yuan HS, Tang H, Shao HZ, Wei DM
This study explored the efficacy and safety of combination pharmacological cardioversion of permanent atrial fibrillation in outpatients following prosthetic mitral valve replacement. The study group comprised 99 outpatients who were randomly divided into two groups. In group 1 (n = 50), only ventricular heart rate was controlled. In group 2 (n = 49), combination pharmacological cardioversion therapy with low-dose oral amiodarone (2 mg/kg), captopril (0.25 mg/kg) and simvastatin (0.3 mg/kg) was administered daily. During 12 months of serial pharmacological treatment, the cardioversion rate was 6% for group 1 and 39% for group 2; the likelihood of cardioversion differed significantly between the two groups. In group 2, one patient developed severe pruritus that necessitated withdrawal from the study and six patients ceased captopril treatment after contracting a persistent cough. In summary, combination pharmacological cardioversion was found to be effective and safe in outpatients who had undergone prosthetic mitral valve replacement.
Captopril decreases plasminogen activator inhibitor-1 in rats with ventilator-induced lung injury.
Crit Care Med. 2008 Jun; 36(6): 1880-5
Chen CM, Chou HC, Wang LF, Lang YD
OBJECTIVE: To test the hypotheses that high tidal-volume ventilation increases plasminogen activator inhibitor (PAI)-1, and the angiotensin-converting enzyme inhibitor, captopril (CAP), may attenuate these effects. SETTING: University research facility. SUBJECTS: Twenty adult male Sprague-Dawley rats. INTERVENTIONS: All rats were randomized to receive two ventilation strategies for 2 h: 1) a high-volume zero positive end-expiratory pressure (PEEP) (HVZP) group at a tidal volume of 40 mL/kg, a respiratory rate of 25 breaths/min, and an FiO2 of 0.21; and 2) an HVZP + CAP group which received an intraperitoneal injection of CAP (100 mg/kg) 30 min before HVZP ventilation. Another group that was not subjected to ventilation served as the control. MEASUREMENTS AND MAIN RESULTS: Total protein recovered from bronchoalveolar lavage fluid was significantly higher in rats ventilated with the HVZP protocols than in control rats. Rats treated with HVZP ventilation had significantly higher lung angiotensin (ANG) II and PAI-1 messenger RNA expression levels and a higher plasma active PAI-1 level than did the control and HVZP + CAP groups. Lung ANG II levels were positively correlated with plasma PAI-1. Representative lung tissue of the HVZP + CAP group showed mild inflammatory cell infiltration and less hemorrhage and fibrin deposition than did the HVZP group. The HVZP and HVZP + CAP groups had significantly higher lung injury scores than did the control group and rats treated with HVZP + CAP ventilation exhibited significantly lower lung injury scores than did the HVZP group. CONCLUSIONS: Mechanical ventilation with a high tidal volume and no PEEP increases alveolar fibrin deposition and systemic PAI-1 activity, which are attenuated by captopril, an angiotensin-converting enzyme inhibitor. These results imply that local ANG II is involved in the pathogenesis of disordered coagulation in ventilator-induced lung injury (VILI) and suggest that the protective mechanism of captopril's attenuation of VILI is related to a reduction in PAI-1.