Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry we investigated the ontogeny of renin, angiotensinogen and angiotensin converting enzyme (ACE) in the mesonephros at 27 and 41 days of gestation, and the metanephros at 41 and 64 days of gestation in ovine fetuses (term is 145 to 150 days). The volume and composition of fetal urine, stored as allantoic fluid were measured in 12 fetuses at 27 days, and 13 fetuses at 41 days. Renin, angiotensinogen and ACE were identified in both meso- and metanephroi at 41 days but not in the mesonephros at 27 to 30 days. Allantoic fluid volumes were 21 +/- 3 and 45 +/- 5 ml at 27 to 30 days and 41 days, respectively. This fluid was significantly different in composition to that of amniotic fluid or maternal plasma. The results suggest that the mesonephros can substantially modify its glomerular filtrate by 27 days of gestation, and can produce local angiotensin II by 41 days.
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PMID:Ontogeny of hormonal and excretory function of the meso- and metanephros in the ovine fetus. 891 29

Renin-angiotensin system plays a prominent role in the sodium and water homeostasis. In addition, activation of renin-angiotensin system frequently occurs in patients with cirrhosis and ascites. Theoretically, administering of angiotensin converting enzyme inhibitors can enhance sodium and water retention in cirrhotic patients with ascites. In this study, we evaluate the role of low-dose captopril on renal function changes, renal plasma flow and hemodynamics in patients with cirrhosis and ascites. Fifty patients are randomly assigned to receive captopril or placebo for 14 days. Renal functions, renal plasma flow, plasma renin activity, plasma aldosterone concentration and systemic and hepatic hemodynamics are measured before and after treatment. Our results indicate that placebo administration did not affect any of the parameter measured in this study. The finding that low-dose captopril significantly increases plasma renin activity suggests that the dose used in this study effectively blocks the enzyme activity. However, low-dose captopril does not affect renal plasma flow, renal functions and systemic and hepatic hemodynamics. Results in this study demonstrate that inhibition of angiotensin converting enzyme alone may not improve sodium and water retention in cirrhotic patients with ascites.
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PMID:Effects of captopril on renal functions, renal and portal hemodynamics in patients with cirrhosis. 893 43

Chronically elevated blood pressure results from pathological alterations in control systems. Current approaches to elucidate the underlying etiology strongly emphasize the (patho)physiological significance of the Renin-Angiotensin-Aldosterone System (RAAS) which interestingly interacts with the sympathetic, the cholinergic and purinergic systems. While the angiotensin-II-receptor subtype 1 (AT1), which mediates the blood-pressure-related effects of angiotensin II (All), has so far been extensively investigated, the physiological relevance of the other angiotensin-II-receptor subtypes-in particular of the AT2-receptor subtype-is about to be evolved by analysis of the various signal transduction mechanisms and by evaluation of transgenic animals, e.g. the knock-out mice, following disruption of the single A-II-receptor subtypes. Based on the clinical success of ACE inhibitors, the blockade of the Renin-Angiotensin-Aldosterone System in many different ways has been recognized as a successful strategy to effectively lower blood pressure.
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PMID:The renin-angiotensin-aldosterone system: focus on its distinct role in arterial hypertension and its various inhibitors as a therapeutic strategy to effectively lower blood pressure. 898 74

We studied the expression of each component of the renin-angiotensin system (renin, angiotensin I-converting enzyme, angiotensinogen, and angiotensin II type I receptor) in balloon-injured rat carotid artery. We assessed the expression levels of the respective mRNAs by competitive polymerase chain reaction. Renin mRNA concentration was markedly increased 24 hours after balloon injury and remained higher than that in the control at 7 days after balloon injury. Angiotensin-converting enzyme mRNA concentration was decreased 24 hours after balloon injury and was increased at 14 days after balloon injury. No significant change in angiotensinogen mRNA concentration was observed throughout the study period. Angiotensin type I receptor mRNA concentration was increased beginning 3 days after balloon injury and remained higher than that in the control at 14 days after balloon injury. Immunohistochemical analysis showed that renin was transiently expressed in medial smooth muscle cells after balloon injury. Administration of quinapril markedly reduced neointimal formation and was accompanied by an attenuation of the increase in the concentrations of angiotensin type I receptor and angiotensin-converting enzyme mRNAs. The upregulation of renin mRNA in balloon-injured rat carotid artery preceded and may play a role in neointimal formation.
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PMID:Induction of renin in medial smooth muscle cells by balloon injury. 909 97

To compare the effects of an angiotensin-converting enzyme inhibitor on circulating and tissue renin-angiotensin system (RAS), we measured different RAS parameters during the first day of treatment (Day1) as well as after two weeks of treatment (Day14). Ramipril was given orally once daily to adult male spontaneously hypertensive rats (SHR). Renin activity (RA), angiotensin converting enzyme (ACE) activity and levels of angiotensin I (ang I) and angiotensin II (ang II) in the plasma, renal cortex and renal medulla were assessed at Day1 and Day14 of the treatment. In the plasma, both RA and ang I increased 10 to 15 fold one to four hours after acute as well as at Day14 of ramipril treatment and then returned to basal values within 24 hours. Plasma ang II levels were not significantly decreased at Day1 or Day14. The decrease in the ang II/ang I ratio suggested a sustained inhibition of plasma ACE at Day14. In the renal cortex and medulla, a clearly different pattern was observed: in ramipril treated rats, RA in the renal cortex and medulla did not change at Day1 but at Day14 we observed a slight and sustained increase in RA. Despite very high basal levels of RA, ang I levels in the renal cortex were comparable to those in the plasma. The ang I level increased only one-fold one hour after ramipril intake at Day1 and Day14. This suggests that angiotensinogen may have a limiting role in the synthesis of ang I in the kidney. Ang II levels were slightly higher in the renal cortex and medulla than in the plasma suggesting local synthesis of the peptide. In the kidney, ang II levels decreased one and four hours after the acute or prolonged ramipril treatment and the ang II/ang I ratio was reduced at the same time. Our results show that the responses of the plasma and kidney components of the RAS to ACE inhibition are different in the plasma and the kidney suggesting that the circulating and tissue RAS are at least in part independent.
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PMID:Renal tissue angiotensins during converting enzyme inhibition in the spontaneously hypertensive rat. 924 47

Congestive heart failure (CHF) patients share several similar features, such as reduced cardiac contractility and neurohumoral activation to compensate the impaired cardiac function. In CHF patients, the cardiac renin-angitensin (RA) system, receptors, GTP-binding proteins, and their effector molecules are inevitably exposed to chronically elevated neurohumoral stimulation. A widely recognized concept is that a chronic increase in such stimulation can desensitize target cell receptors and the post-receptor signal transducing pathway. Recently, reports of several studies have indicated that the inhibitory GTP-binding protein (Gi) can be increased in CHF patients and animal models. Although direct evidence for a change in catalytic protein of adenylyl cyclase has not been found, limited information has suggested a reduced catalytic activity in terminally failing hearts. In this paper, we have assessed the changes in beta AR, GTP-binding protein, catalytic protein and beta ARK. We also examined angiotensinogen mRNA expression in failing heart. It was detected not only in the liver, but also in both the atrial and ventricular heart tissues, suggesting that angiotensinogen is synthesized in the human heart. Immunohistochemical studies revealed a stronger reaction in the endocardial layer of the human left ventricle than in the epicardial layer, and intense immunoreactivity in the conduction system and right atrium. Our experiments revealed a widespread immunopositive reaction for angiotensinogen in the left ventricle of diseased hearts. In the non-diseased heart, ACE and AT1 receptor RNA are present in ventricular muscles. Renin and Ao mRNA could not be detected in the subendocardium of non-diseased left ventricle, but both were present in the left ventricle of diseased hearts. These data indicate that the cardiac RA system plays an important role in the deterioration of cardiac function.
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PMID:Alterations of signal transduction system in heart failure. 929 May 67

This study investigated the drinking response and the expression of Fos- and Egr-1-immunoreactivity (Fos-ir; Egr-1-ir) in the brain induced by endogenous angiotensin generated by intracerebroventricular (i.c.v.) injection of renin. Renin induced Fos-ir in the subfornical organ (SFO), median preoptic (MnPO), supraoptic and paraventricular nuclei (SON and PVN), area postrema (AP), nuclei of the solitary tract (NTS) and lateral parabrachial nuclei (LPBN). Renin-induced Egr-1-ir exhibited a similar pattern of distribution as that observed for Fos-ir. The dose of i.c.v. renin that induced expression of immediate early gene (IEG) product immunoreactivity also produced vigorous drinking. When renin-injected rats were pretreated with captopril, an angiotensin converting enzyme inhibitor, drinking was blocked. With the same captopril pretreatment, both Fos- and Egr-1-ir in the SFO, MnPO, SON, PVN, AP and LPBN were also significantly reduced.
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PMID:Central renin injections: effects on drinking and expression of immediate early genes. 951 46

Renin-angiotensin system promotes sodium and chloride retention, participates in the defense response to hypovolemia and, in congestive heart failure, contributes to edema formation and progression of the disease. We investigated whether ACE-inhibitors interfere with the action of the renin-angiotensin system on the nephron, and therefore with water and urinary electrolytes excretion. The interaction among renin-angiotensin system, diuretic treatment and urinary electrolytes was evaluated both during chronic treatment and in response to acute renin-angiotensin system activation as that observed after extracorporeal ultrafiltration-induced transient hypovolemia. Plasma renin activity and aldosterone, body fluid balance and urinary sodium, chloride and potassium concentrations were evaluated in 30 patients with congestive heart failure in NYHA II-III functional class, grouped according to whether long-term therapy did not include (Group I, n = 15) or included (Group II, n = 18) ACE-inhibitors. All parameters were evaluated at baseline and after a single session of extracorporeal ultrafiltration. At baseline, urinary output and urinary sodium and chloride concentrations were similar in the two groups, while urinary potassium concentration was lower in patients assuming ACE-inhibitors (Group II). Plasma renin activity was higher and aldosterone was lower in Group II than in Group I. After removal of similar amounts of plasma water by extracorporeal ultrafiltration, body weight decreased in both groups but the decrease was maintained in the following days only in Group II patients. A transient reduction (48 hours) of both plasma volume and urinary output was observed after ultrafiltration in both groups. Despite plasma renin activity and aldosterone increase, urinary electrolytes response to ultrafiltration was different in the two groups: sodium and chloride were reduced, and potassium did not change in Group 1 while, in Group II, sodium and chloride did not change and potassium excretion was significantly increased. In conclusion, chronic treatment with ACE-inhibitors does not enhance the excretion of sodium in congestive heart failure but just mitigates potassium loss. The role of these drugs becomes particularly relevant during acute renin-angiotensin system activation due to hypovolemia; in this setting ACE-inhibitors counteract sodium and chloride retention resulting in a potential hazard due to interference with the defence mechanisms toward hypovolemia, and an amplification of extracorporeal ultrafiltration efficacy by preventing edema recovery after its mechanical removal.
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PMID:[The influence of ACE inhibitors on urinary electrolyte secretion and the response to transitory hypovolemia in chronic heart failure]. 953 23

1. The concentration of renin and angiotensinogen (Ao) and the activity of angiotensin I-converting enzyme (ACE) was measured in the ascites fluid of nephrotic rats obtained 8 days after puromycin aminonucleoside (PAN) injection. 2. Ascites fluid, serum and urine proteins of these rats were analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). 3. Renin, Ao and ACE were found in the ascites fluid and the percentage of the ratio ascites fluid/(plasma or serum) ranged from 5.9 to 9.9%. The electrophoretic analysis revealed that the ascites fluid contained low (Mr < 66 kDa) and high (Mr < 66 kDa) molecular weight proteins. Albumin and six proteins higher than 66 kDa were present both in the ascites fluid and in serum from nephrotic rats. 4. Data from the study suggest that some proteins in the ascites fluid, including renin, Ao and ACE, come from the plasma. It is possible that the loss of renin, Ao and ACE to the ascites fluid may be playing a role in the metabolic alterations of these three proteins in PAN-nephrotic rats.
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PMID:Ascites fluid of nephrotic rats: sodium dodecyl sulphate-polyacrylamide gel electrophoresis protein pattern and the renin-angiotensin system. 967 30

Concomitant arterial hypertension and metabolic disorders is a frequent finding raising the risk of micro- and macrovascular complications. While prevalence of stroke and myocardial infarction is going down in hypertensives, end-stage renal disease (ESRD) becomes a bigger problem especially in diabetic hypertensives. The metabolic abnormalities are linked to the hypertension by the sympathoadrenal system mediated by insulin resistance (IR); subjects with hyperinsulinemia and increased sympathetic activity tend to have higher blood pressure, typical dyslipidemia, reduced fibrinolytic activity and other risk factors (RF) called metabolic syndrome of IR. Albuminuria (AUR) is considered as an important RF for the development of nephropathy, ESRD, cardiovascular diseases. AUR is a marker of cardiovascular and total mortality in diabetic and/or non-diabetic hypertensives. AUR reflects the endothelial dysfunction not only in glomerulus but also in the other arteries. Tissue Renin-Angiotensin System plays a significant role in the pathogenesis of hypertension and metabolic disorders; it affects the arterial wall, kidneys and heart longitudinally. Life style is very essential in the treatment of hypertension and metabolic disorders: rational diet with reduced amount of salt and animal proteins, non-smoking and sufficient physical activity. Antihypertensive drugs without any metabolic side effects and with the renal protection are necessary for the patients with hypertension and metabolic disturbances. ACE-inhibitors and/or some of the Ca-antagonists seems to be valuable especially as combined therapy.
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PMID:[New approaches in the treatment of hypertension in metabolic diseases]. 972 74


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