Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether angiotensin converting enzyme inhibition could ameliorate renal ischemic injury. Both a chronic rat model and a rat isolated perfused kidney (IPK) model were used. Adult rats were subjected to 60 min of left hilar crossclamping and right nephrectomy. Captopril (1 mg/kg) was given intravenously 5-10 min prior to clamping (CAP-pre, n = 5), at reperfusion (CAP-post, n = 5), or 30 min after reperfusion (CAP-30 min post, n = 5). Other groups of rats received enalapril (0.8 mg/kg iv) in the same manner (ENAL-pre, n = 5; ENAL-post, n = 5; ENAL-30 min post, n = 4). Serum creatinine in the treated groups was compared to ischemic control (NS, n = 7) for 7 days. In the IPK experiments, kidneys were similarly treated with CAP or ENAL. Vascular resistance (VR) and oxygen consumption (O2 CON) were determined from pressure, flow, and oxygen tension data for 60 min after initial equilibration. In the chronic model, Day 2 serum creatinine was significantly lower in all treated groups vs ischemic control. By Day 7, serum creatinine remained significantly lower in all ENAL-treated groups and in the CAP-30 min post group, although other CAP-treated groups had appreciably, although not significantly, lower creatinines, too. Histologic examination of CAP-pre kidney revealed intact morphology compared to ischemic control where acute tubular necrosis was observed. In the IPK experiments, CAP- and ENAL-treated kidneys had VR values that were significantly lower than those of ischemic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Captopril amelioration of renal reperfusion injury. 804 Nov 45

The purpose of the present study was to separately investigate the effects of two different dosages of captopril on pressor, vascular and humoral response to acute extracellular volume expansion in patients with borderline hypertension (BHT). Thirty-five patients were randomly allocated in two groups undergoing acute saline infusion (0.40 ml/min/kg for 45 min and 0.15 ml/min/kg for 75 min)before and after a 7-day period of treatment with either placebo or captopril at the dose of 12.5 (LD-CAP) or 50 mg (HD-CAP) twice a day. At baseline the effects of LD-CAP were limited to an increase in PRA and to a decrease in plasma aldosterone whereas HD-CAP decreased systolic and diastolic blood pressure (SBP, DBP), forearm vascular resistance (FVR) and increased venous distensibility (VV(30)) as well. After saline loading patients treated with HD-CAP showed an increase in SBP, DBP not observed in patients allocated to LD-CAP. Urinary sodium excretion in response to NaCl loading was selectively enhanced by LD-CAP (+25%) whereas HD-CAP did not (+6.3%). The present data suggest that low-doses of ACE-inhibitors acting through a selective blockade of RAA not associated with hemodynamic changes can enhance the natriuretic response to acute volume expansion in borderline hypertensives.
 ...
PMID:Low dose of ACE-inhibitor enhances sodium excretion in volume expanded patients with borderline hypertension. 886 99

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an alpha-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 microg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.
 ...
PMID:Pulmonary edema induced by angiotensin I in rats. 951 4

The long-term administration of captopril to patients with a left ventricular dysfunction after myocardial infarction reduces the rate of recurrent coronary thrombosis. Thus, in the present study we investigated the influence of angiotensin-converting enzyme inhibitors (ACE-Is) on experimental venous thrombosis in normotensive rats and the involvement of NO and PGI2 in this effect. Animals were treated with captopril (1.5, 5 or 25 mg/kg twice daily, CAP), enalapril (15 mg/kg once daily, ENA) or distilled water for 10 days, per os. After ligation of the vena cava the thrombus weight decreased in both CAP and ENA treated rats. The effect was most pronounced in animals given the highest dose of CAP (p<0.0001 vs. control) and was significantly stronger than observed in ENA treated animals (CAP vs. ENA p<0.01). The mean blood pressure measured by the "tail cuff" method and platelet aggregation were not altered by either of the ACE-Is. The antithrombotic activity of CAP was reduced by indomethacin (2.5 mg/kg, s.c.) and independently by the NO-synthase inhibitor N(G)-nitro L-arginine methyl ester (3 mg/kg i.v. bolus + 3 mg/kg/h i.v. infusion, L-NAME). In the latter case CAP regained its antithrombotic properties in rats pretreated with L-Arginine (300 mg/kg i.v. + 300 mg/kg/h i.v.) before administration of L-NAME (p<0.05 vs. control). Moreover, the concomitant administration of indomethacin and L-NAME failed to completely abolish the antithrombotic action of captopril. Similar effects were observed in respect to the incidence of venous thrombosis. Our study documents a novel and important effect of ACE-Is on the vein thrombotic process and demonstrates the involvement of NO and PGI2 in this phenomenon.
 ...
PMID:Nitric oxide and prostacyclin are involved in antithrombotic action of captopril in venous thrombosis in rats. 965 49

Cystinyl aminopeptidase (CAP; EC 3.4.11.3) is an integral protein of the placental membrane that is also found in a soluble form in maternal serum during pregnancy. CAP was found to be shed from human placental membranes in a temperature- and time-dependent process. The released form of CAP was hydrophilic as assessed by phase separation in Triton X-114 and high-speed centrifugation. This ectodomain shedding of CAP was inhibited by the hydroxamic acid-based compounds marimastat and BB3103. The inhibition profile for the shedding of CAP was distinct to that for the release of angiotensin converting enzyme, implicating the involvement of distinct zinc metallosecretases in the shedding of these two proteins. These results have implications for our understanding of the mechanism underlying the reduction in serum levels of CAP observed in certain pregnancy-related disorders, such as pre-eclampsia.
 ...
PMID:Ectodomain shedding of cystinyl aminopeptidase from human placental membranes. 1186 93

The present study was carried out to investigate whether 0.3 M NaCl and water intake alters the release of serotonin (5-hydoxytryptamine, 5-HT) in the region of the lateral parabrachial nucleus (LPBN) in freely moving rats. The ingestion of 0.3 M NaCl and water was induced by subcutaneous injections of the diuretic furosemide (FURO, 10 mg/kg) and the angiotensin converting enzyme inhibitor captopril (CAP, 5 mg/kg), and extracellular concentrations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) were measured using intracerebral microdialysis techniques. The intake of 0.3 M NaCl and water significantly enhanced the 5-HT and 5-HIAA levels in the LPBN area. The combined treatment with FURO and CAP elicited significant decreases in the 5-HT and 5-HIAA concentrations in the LPBN area under the condition that 0.3 M NaCl and water are not available for drinking. These results suggest that the serotonergic system in the LPBN area may play an important role in the modulation of sodium appetite and thirst.
 ...
PMID:Involvement of serotonergic systems in the lateral parabrachial nucleus in sodium and water intake: a microdialysis study in the rat. 1503 9

Microdialysis was employed to investigate whether N-methyl-d-asparatate (NMDA) glutamate receptor mechanisms are involved in the modulation of serotonin (5-hydoxytryptamine, 5-HT) release in the region of the lateral parabrachial nucleus (LPBN) in freely moving rats. Perfusion of NMDA (10 and 50 microM) through the microdialysis probe significantly enhanced extracellular concentrations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the LPBN area. Local perfusion of the NMDA antagonist dizocilpine (MK801, 10 and 50 microM) did not change the basal 5-HT and 5-HIAA levels in the LPBN area. MK801 (10 microM) administered together with NMDA antagonized the stimulant effect of NMDA (10 microM). The intake of 0.3M NaCl and water induced by subcutaneous injections of the diuretic furosemide (FURO, 10 mg/kg) and the angiotensin converting enzyme inhibitor captopril (CAP, 5 mg/kg) produced significant increases in the 5-HT and 5-HIAA concentrations in the LPBN area. The increased levels of 5-HT and 5-HIAA caused by the combined treatment with FURO and CAP were attenuated by perfusion of MK801 (10 microM). These results indicate the participation of NMDA receptors in the control of 5-HT release in the LPBN area.
 ...
PMID:Involvement of NMDA receptor mechanisms in the modulation of serotonin release in the lateral parabrachial nucleus in the rat. 1711 61

The objective of this study was to find out if lipopolysaccharide (LPS) administered intraperitoneally affects sodium and water intake and renal excretion in dehydrated rats. LPS (0.3-5 mg/kg b.w.) inhibited 0.3M NaCl intake induced by subcutaneous injection of the diuretic furosemide (FURO, 10 mg/kg b.w.) combined with the angiotensin converting enzyme inhibitor, captopril (CAP, 5 mg/kg b.w.). Only the highest doses of LPS (2.5 and 5 mg/kg) inhibited water intake induced by FURO/CAP. LPS (0.6 mg/kg) reduced urinary volume and sodium excretion, but had no effect on mean arterial pressure or heart rate of rats treated with FURO/CAP. LPS (0.3-5.0 mg/kg) abolished intracellular thirst and reduced by 50% the urine sodium concentration of rats that received 2 ml of 2M NaCl by gavage. LPS (0.3-5.0 mg/kg) also reduced thirst in rats treated with FURO alone (10 mg/rat sc). The results suggest that LPS has a preferential, but not exclusive, inhibitory effect on sodium intake and on intracellular thirst. The inhibition of hydro-mineral intake and the antinatriuresis caused by LPS in dehydrated rats may contribute to the multiple effects of the endotoxin on fluid and electrolyte balance and be part of the strategy to cope with infections.
 ...
PMID:Lipopolysaccharide reduces sodium intake and sodium excretion in dehydrated rats. 2097 13

The evaluation of some indicators of blood proteolytic systems and their role in the development of endothelial dysfunction in noninflammatory form of chronic prostatitis abacterial (CAP III B) was performed. The association between the activity of blood proteolytic systems and endothelial damage in patients with CAP III B was examined. Indicators of blood kallikrein-kinin system and renin-angiotensin system (activity of kallikrein, alpha1-proteinase inhibitor, alpha2-macroglobulin, total argininesterase activity, activity of angiotensin converting enzyme, prekallikrein content) were evaluated in 32 patients with CAP III B before and after occlusive bronchial test. It was established that a violation of endothelium-dependent vasodilation is accompanied by an imbalance of pro- and antiproteolitic blood systems.
 ...
PMID:[The role of endothelial dysfunction in the pathogenesis of non-inflammatory form of chronic abacterial prostatitis]. 2398 47

Previous studies have shown that the subfornical organ (SFO) is involved in the modulation of sodium intake in rats. To clarify whether serotonergic mechanisms in the SFO participate in the modulatory system, the present study was carried out to examine the effects of sodium and water intake on serotonin (5-hydroxytryptamine, 5-HT) release in the subfornical organ (SFO) in freely moving rats. The ingestion of 0.3M NaCl and water was induced by subcutaneous injections of the diuretic furosemide (FURO, 10mg/kg) and the angiotensin converting enzyme inhibitor captopril (CAP, 5mg/kg), and extracellular concentrations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the region of the SFO were measured using intracerebral microdialysis techniques. The combined treatment with FURO and CAP elicited significant decreases in the 5-HT and 5-HIAA levels in the SFO area. The 0.3M NaCl and water intake caused by the treatment significantly enhanced the 5-HT and 5-HIAA concentrations in the SFO area compared with the basal levels. No significant changes in the 5-HT and 5-HIAA levels caused by either the FURO and CAP treatment or water and NaCl intake were observed in the sites away from the SFO. These results suggest that the serotonergic mechanism in the SFO may be important for the control of sodium appetite and thirst.
 ...
PMID:Serotonin release in the subfornical organ area induced by sodium and water intake in the rat. 2711 15


1