Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, we examined the effect of blockade of the brain stem renin-angiotensin system on renal sympathetic baroreflexes and chemoreflexes in conscious rabbits and examined the role of central catecholaminergic pathways in these responses. Eleven rabbits underwent preliminary surgical instrumentation and pretreatment with central 6-hydroxydopamine (6-OHDA, 500 micrograms/kg) or ascorbic acid 6 wk before the commencement of the experiments. Baroreflex curves were determined under conditions of normoxia and hypoxia (10% O2 + 3% CO2) before and after central administration of either Ringer solution, the ANG II receptor antagonist losartan (10 micrograms), or the angiotensin-converting enzyme inhibitor enalaprilat (500 ng) on separate days. Losartan increased the upper plateau and the range of the mean arterial pressure (MAP)-renal sympathetic nerve activity (RSNA) curve (79 and 78%, respectively) in intact rabbits, whereas this effect was not observed in 6-OHDA-pretreated rabbits. Hypoxia elicited an increase in resting RSNA (111% in intact rabbits and 74% in 6-OHDA-injected rabbits) and elevated the upper plateau of the RSNA-MAP curve in both groups (89% in intact rabbits and 114% in 6-OHDA-injected rabbits). During hypoxia, losartan and enalaprilat increased the RSNA upper plateau in intact rabbits but had no effect in 6-OHDA-pretreated rabbits. No effects on the MAP-heart rate baroreflex curves were observed. Thus the effect of losartan to increase RSNA, particularly during hypoxia and baroreceptor unloading, being abolished by central noradrenergic depletion suggests that the endogenous ANG II which normally causes an inhibition of renal sympathetic motoneurons is dependent on the integrity of central catecholaminergic pathways.
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PMID:Role of central catecholaminergic pathways in the actions of endogenous ANG II on sympathetic reflexes. 975 48

This article describes a model of the human circulatory system, with emphasis on metabolic processes in particular the calculation of CO2 balance and the pH of venous blood. The model overall is capable of simulating both physiological and pathological circulatory systems. Simulated parameters are locally distributed blood flows, and pressures in the arterial system. This modelling of haemodynamics serves, among other things, to determine the oxygen supply situation of individual organs. The four most important control mechanisms of the human circulatory system for maintaining haemodynamics--the renin-angiotensin system, the autonomic nervous system, local arterial autoregulation and vascular stress relaxation--have been incorporated into the model. Another important parameter for estimating the oxygen supply situation of the human body is the acid-base status of arterial and venous blood. The calculation of the pH of blood plasma and erythrocytes is described in the second part of the article. The results achieved with our simulation model correspond well with those reported in the literature. The behaviour of the human circulatory system can be reproduced at rest and under conditions of loading.
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PMID:[Simulation of metabolic processes in human circulation: evaluation of pH value and CO2 balance]. 984 43

This study was undertaken in order to determine whether or not the increased intra-abdominal pressure during laparoscopic procedures causes renal ischaemia and parenchymal pathology. Fifteen adult New Zealand rabbits were used in the study. Anaesthesia was maintained by 2% isoflurane, 50% O2 in air. Heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), end-tidal carbon dioxide (PETCO2), airway pressure (Paw) and blood gases were monitored. Rabbits in control group (group C, n = 7) and study group (group S, n = 8) had a Veress needle placed supraumbilically. Group S was insufflated with CO2 sequentially at 5, 10 and 15 mmHg of intra-abdominal pressures (IAP); each pressure level was maintained for 20 minutes. At the end of the study, laparotomy was performed and blood was withdrawn from renal vein for measurements of renin and angiotensin I levels, and the other kidney was removed simultaneously for pathological evaluation. Haemodynamic and respiratory measurements were stable in group C and were variable in group S. The renin level was 7.27 +/- 0.34 ng.mL-1 and angiotensin I was 5.01 +/- 0.32 ng.mL-1 in group C. In group S, levels of renin and angiotensin I were 26.2 +/- 5.9 ng.mL-1 and 39.4 +/- 12.1 ng.mL-1 respectively, being significantly higher than group C (p < 0.05). Pathological scores were 0.02 +/- 0.008 in group C and 0.82 +/- 0.124 in group S (p < 0.05). There were significant histological changes in group S compared with group C. During prolonged laparoscopic operations high intra-abdominal pressures may result in intra-abdominal organ ischaemia.
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PMID:An experimental study on the relationship of intra-abdominal pressure and renal ischemia. 1128 Oct 48

This study was designed to test the hypothesis that increased pressure itself could cause endothelial dysfunction and lead to decreased nitric oxide (NO) release, partly through effects on the tissue renin angiotensin system in hypertension. Cultured endothelial cells (ECs) isolated from the aortas of WKY rats were continuously exposed to a pressure of 150 mmHg in a CO2 incubator for 72 h using a pressure system, and the NOx (NO2 and NO3) and angiotensin II (Ang II) concentrations in the supernatant were measured. An Ang II type 1 receptor (AT1R) antagonist (losartan) and an Ang II type 2 receptor (AT2R) antagonist (PD123319) were added to the medium. The expression of AT1R and AT2R mRNAs was also examined. Pressure loading significantly decreased the NO release from ECs. Concomitant administration of losartan restored NO release to the level before the application of pressure (p<0.001). This effect of losartan was blocked by simultaneous administration of PD123319, bradykinin type 2 receptor antagonist, and NO synthase inhibitor (p<0.05). The Ang II concentration was increased by pressure and was further increased by losartan. The gene expression of AT1R was not changed by pressure, but AT2R mRNA was increased almost 2-fold. These results indicate that high pressure itself attenuates NO release from ECs, and that losartan improves NO release by activating the bradykinin system via AT2R stimulation. In addition, the increase of AT2R gene expression in ECs during exposure to pressure may compensate for the reduction of NO.
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PMID:Contrasting effects of angiotensin type 1 and 2 receptors on nitric oxide release under pressure. 1245 33

In rat outer medullary collecting duct (OMCD), the mechanism(s) and regulation of H+ secretion are not understood fully. The effect of changes in acid-base balance and the renin-angiotensin system on net H+ secretion was explored. Rats received NaCl, NaHCO3, NH4Cl, or nothing in their drinking water for 7 days. Total ammonia and total CO2 (JtCO2) fluxes were measured in OMCD tubules perfused in vitro from rats in each treatment group. JtCO2 was reduced in tubules from rats drinking NH4Cl relative to those drinking NaHCO3. Because NH4Cl intake increases plasma renin and aldosterone, we asked if upregulation of the renin-angiotensin system reduces net H+ secretion. Deoxycorticosterone pivalate administered in vivo did not affect JtCO2. However, ANG II given in vivo at 0.1 ng/min reduced JtCO2 by 35%. To determine if ANG II has a direct effect on acid secretion, JtCO2 was measured with ANG II applied in vitro. ANG II (10-8 M) present in the bath solution reduced JtCO2 by 35%. This ANG II effect was not observed in the presence of the AT1 receptor blocker candesartan. In conclusion, in rat OMCD, JtCO2 is paradoxically reduced with NH4Cl ingestion. Increased circulating ANG II, as occurs during metabolic acidosis, reduces JtCO2.
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PMID:ANG II reduces net acid secretion in rat outer medullary collecting duct. 1285 Dec 54

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.
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PMID:Association of Bartter's syndrome and empty sella. 1451 87

Water retention and hyponatraemia are typically observed in the final stages of Chronic Obstructive Pulmonary Disease (COPD) and the onset of edema is a poor prognostic factor. For several years the pathogenesis of edema in COPD patients was attributed to heart impairment because of pulmonary hypertension, but the evidence that cardiac output is often adequate for the metabolic demands has suggested, since 1960, that the pathogenesis of edema in these patients would be correlated with gas exchange impairment and in particular with carbon dioxide (CO2) retention. The gas exchange impairment induces, in these patients several hormonal abnormalities: renin (Rn), angiotensin II (AnII), aldosterone (Ald), atrial natriuretic peptide (ANP), vasopressin (ADH) and endothelial factors are some of the factors involved. The systemic response to hypercapnia has the effect of reducing the renal blood flow and, as a result, increasing water and sodium retention with the final effect of edema and hyponatraemia. The aim of this brief review is to highlight the current knowledge on renal/hormonal abnormalities in COPD and their therapeutic implications.
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PMID:Water and sodium imbalance in COPD patients. 1551 Jul 11

Atherosclerotic renal artery stenosis (RAS) is relatively common and often associated with reversible hypertension, progressive renal insufficiency, and/or coronary-independent pulmonary edema. Not all RAS is associated with renovascular hypertension. Historical and physical findings may suggest renovascular hypertension and warrant investigation for RAS. Noninvasive diagnostic imaging options include renal artery duplex ultrasonography, magnetic resonance angiography, computed tomographic angiography, and CO2 angiography, with each method having its own advantages and limitations. Functional tests of renal flow, which characterize RAS significance, include captopril-stimulated plasma renin activity and captopril renography. To date, no single approach has shown clear superiority either in diagnosis or identification of patients most likely to benefit from revascularization. Revascularization of RAS is recommended for severe/drug-refractory hypertension, preservation of renal function, recurrent flash pulmonary edema, or recurrent severe heart failure. Intervention response is variable, but the ongoing Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial, comparing medical therapy with and without stenting, should provide management guidance.
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PMID:Atherosclerotic renal artery stenosis and renovascular hypertension: clinical diagnosis and indications for revascularization. 1684 4

Acute carbon dioxide (CO2) poisoning causes no specific features that are revealed upon autopsy, and the pathophysiological mechanism of this syndrome is unclear. To address this issue, in the present study, we exposed rats to CO2 concentrations ranging from 10% to 60% and determined the effects on mRNA expression. According to the results of Gene Ontology (GO) and cluster analyses of microarrays data, we selected the following genes for further analysis: alkylglycerone phosphate synthase (Agps), hypocretin (Hcrt), tyrosine hydroxylase (Th), heat shock protein beta 2 (Hspb2), and opioid receptor delta 1 (Oprd1) expressed in the frontal cortex and renin (Ren), pancreatic polypeptide (Ppy), corticotropin releasing hormone receptor 2 (Crhr2), carbonic anhydrase 1 (Car1), and hypocretin receptor 1 (Hcrtr1) expressed in the hypothalamus. We found significant differences between the expression levels of Agps and Hspb2 mRNAs in the frontal cortex and that of Ppy, Crhr2 mRNAs in the hypothalamus in the presence of high concentrations of CO2. Further investigation of these genes may clarify the pathophysiology of acute CO2 poisoning and facilitate the development of novel forensic tests that can diagnose the cause of death.
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PMID:Expression of mRNA in the frontal cortex and hypothalamus in a rat model of acute carbon dioxide poisoning. 2625 16


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