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)

In chloralose-anesthetized dogs, we investigated the disappearance of bradykinin on passage across the renal circulation. The peptide was infused into a renal artery at various doses (5-200 ng/kg min-1); renal blood flow and the concentration of kinins in renal venous blood were then determined and the percent survival of bradykinin on passage through the kidney calculated. Bradykinin caused a dose-related increase in renal blood flow, urine flow, sodium excretion, and kinin content of renal venous blood. Intravenous administration of BPP9alpha (300 mug/kg), a peptide kininase II inhibitor, potentiated the renal vasodilator, diuretic, and natriuretic actions of bradykinin and augmented the survival of the kinin on passage through the kidney from 12.72 +/- 1.64% in control dogs to 53.92 +/- 7.48% (P less than 0.001). Furthermore, the values of peptide survival were positively correlated with the increases in renal blood flow (r = 0.92, P less than 0.01), urine flow (r = 0.75, P less than 0.01), and sodium excretion (r = 0.68, P less than 0.01) produced by bradykinin. In addition, BPP9alpha by itself increased renal blood flow (16%, P less than 0.01), urine flow (115%, P less than 0.005), and sodium excretion (167%, P less than 0.02). Similarly, the concentration of kinin in renal venous blood and the excretion of urinary kinins rose from 0.11 +/- 0.03 ng/ml and 4.1 +/- 1.1 ng/min to 0.24 +/- 0.05 ng/ml (P less than 0.005) and 38.5 +/- 12.2 ng/min (P less than 0.02). These studies suggest that kinins generated intrarenally play a role in the regulation of renal blood flow and salt-water excretion and that variations in the capacity of the kidney to inactivate kinins may be a determinant of the intrarenal activity of the kallikrein-kinin system.
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PMID:Disappearance of bradykinin in the renal circulation of dogs. Effects of kininase inhibition. 16 99

The effect of acute administration of SQ 14,225, a new angiotensin converting enzyme inhibitor, on the drinking response of female rats administered either isoprenaline, angiotensin I, or angiotensin II was studied during 2 h after treatment. Administration of isoprenaline (25 micrograms/kg body wt) was accompanied by a significant increase in water intake when compared with saline-treated controls. Acute administration of a constant dose of isoprenaline (25 micrograms/kg body wt) and increasing doses of SQ 14,225 (5--50 mg/kg) was accompanied by a dose-related, linear decrease in water intake. Acute administration of either angiotensin I or angiotensin II (200 micrograms/kg body wt) was accompanied by a significant increase in water intake. The dipsogenic response to angiotensin II was not affected by acute administration of 35 mg SQ 14,225/kg body wt. However, at the same dose of SQ 14,225, angiotensin I-induced thirst was attenuated. Since isoprenaline-induced and angiotensin I-induced, but not angiotensin II-induced, thirsts are blocked by SQ 14,225, the results suggest that isoprenaline-induced thirst is mediated by way of the renin--angiotensin system.
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PMID:Effect of an angiotensin converting enzyme inhibitor (SQ 14,225) on beta-adrenergic and angiotensin-induced thirsts. 22 56

Urines and sera (human, guinea pig and rat) contain low molecular weight inhibitors of angiotensin converting enzyme (ACE). The urines contain ACE, but the enzyme is scarcely measurable without prior ultrafiltration or dialysis. The activity increases strikingly through three ultrafiltration steps using a membrane with a 10,000 MW retention limit. As implied, the ultrafiltrates contain inhibitory activity and can prevent the hydrolysis of [3H]benzoyl-Gly-His-Leu by ACE from any source, including lung and serum. Human urinary ultrafiltrate contains at least three inhibitors separable on Bio-Gel P-2. The inhibitors are acidic and can be partially purified on Bio-Rex 70 developed with an acetic acid gradient. The smallest of the inhibitors can be purified to apparent homogeneity by partition chromatography (sephadex G-25; butanol, acetic acid, H2O; 4:1:5). The excretion of inhibitory activity varies in response to dietary salt: Activity is low when rats are maintained on a high NaCl diet and is high (3 x's control) on a low NaCl diet. Thus, the activity of ACE may be modulated in vivo by naturally-occurring enzyme inhibitors. Whether some hypertensive patients are deficient in ACE inhibitory activity remains to be determined.
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PMID:Mammalian inhibitors of angiotensin converting enzyme (kininase II). 22 13

1. Isoprenaline hydrochloride injected subcutaneously in rats given a choice test of 1.8% NaCl and water, first induced saline intake which started immediately and was almost concluded in 15 min, followed by a copious water intake. When either saline or water were given in a separate test, saline intake surpassed the water intake in the first 15 min.2. The delay of 15, 30 or 60 min after injection of isoprenaline, 100 mug/kg, before drinking was allowed, significantly reduced saline intake but did not modify the amount of water subsequently drunk.3. Isoprenaline caused a sudden drop in arterial blood pressure, the extent and duration depending on the dose. The time of maximum drop 3-4 min after injection coincided with the time the rat drank salt.4. Isoprenaline-induced saline drinking was significantly reduced after bilateral nephrectomy but water intake was unaffected.5. The beta-adrenoceptor blocking agent, propranolol, inhibited isoprenaline-induced NaCl and water intake, while the alpha-adrenoceptor antagonist phenoxybenzamine abolished isoprenaline-induced NaCl intake and enhanced water intake.6. Saralasin acetate (P-113), a competitive inhibitor of angiotensin II, given into the third brain ventricle, prevented the isoprenaline-induced NaCl and water intake as well as angiotensin II-induced drinking. The angiotensin converting enzyme inhibitor SQ-20881 reduced the isoprenaline-induced NaCl and water intake.7. In conclusion, hypotension might be a component of salt drinking evoked by isoprenaline although the dipsogenic action of beta-stimulation is mainly due to endogenous renin-angiotensin activation.
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PMID:Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists. 23 Nov

The spontaneous water intake of rats increases when they are transferred abruptly from a cold (5 degrees C) to a neutral (25 degrees C) environment. This has been termed thermogenic drinking. Treatment of cold-acclimated rats with SQ 14,225, an angiotensin converting enzyme inhibitor, at 10-50 mg/kg of body weight prior to removal from cold, inhibited the thermogenic drinking response in a dose-dependent manner. Plasma for determination of plasma renin activity (PRA) was obtained by cardiac puncture from methoxyflurane anesthetized rats maintained chronically at both 25 degrees and 5 degrees C. In addition, plasma was obtained from cold-acclimated rats 15 min after removal from 5 degrees to 25 degrees C. PRA values were 2.2 +/- 0.4 (S.E.) ng/ml/h for control rats; 1.9 +/- 0.8 ng/ml/h for cold-acclimated rats and 8.5 +/- 1.7 ng/ml/h for cold-acclimated rats removed from cold for 15 min. Thus, PRA was significantly increased in rats removed acutely from cold. These data suggest that thermogenic drinking may be mediated by the renin-angiotensin system.
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PMID:Relationship between thermogenic drinking and plasma renin activity in the rat. 38 90

To determine the effect of chronic alcohol ingestion, rats were given 15 or 25% v/v of alcohol in water for a period of 6 months. The activities of some key enzymes involved in the metabolism of glucose, mitochondrial respiratory rates, and efficiency of oxidative phosphorylation were studied in the hearts of alcohol-treated and untreated rats. In the group receiving 15% alcohol, glucose-6-phosphate dehydrogenase (G-6-PDH) was elevated. In rats given 25% alcohol, activities of G-6-PDH, aldolase, and glyceraldehyde phosphate dehydrogenase were elevated but isocitrate dehydrogenase was reduced. Mitochondrial respiratory rates and the efficiency of phosphorylation were depressed in rats given 25% of alcohol. Except for mitochondrial oxidation of pyruvate and alpha-ketoglutarate, all biochemical parameters studied were within normal limits a month after alcohol was discontinued.
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PMID:The effect of chronic ethanol ingestion on myocardial glucose and energy metabolism. 56 91

1. Glucose absorption, water absorption and dipeptide hydrolase activities have been determined in isolated rat small intestine at 1, 3, 5 and 21 days after a single intraperitoneal injection of 5-fluorouracil. 2. Absorption rates and enzyme activities were elevated 1 day after treatment, but were reduced to 40% of control values at 3 and 5 days. Changes were seen regardless of whether absorption was expressed per unit length or per unit dry weight of intestine. 3. There were highly significant positive correlations between glucose or water absorption rates and peptidase activities, especially in proximal jejunum. The most significant correlation was observed between water absorption rate and jejunal L-Leu-Gly hydrolase activity. 4. Malabsorption may account for some of the gastrointestinal side effects associated with treatment with 5-fluorouracil. Enzyme measurements may be useful as an index of intestinal function.
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PMID:Changes in absorptive and peptide hydrolase activities in rat small intestine after administration of 5-fluorouracil. 63 72

Kinins and prostaglandins of the E series (PGE) have the capacity to influence renal hemodynamic and excretory events and may interact intrarenally so as to reinforce one another. Thus, in the isolated Krebs-perfused rabbit kidney we showed that addition of either bradykinin or kininogen to the perfusing fluid augments the release of a PGE-like substance and that aprotinin, a kallikrein inhibitor, reduces the release of prostaglandins evoked by kininogen but not by bradykinin. Moreover, we have observed that deoxycorticosterone, an agent which increases urinary kallikrein, enhances the urinary excretion of PGE-like substance, and that this effect is prevented by simultaneous treatment with aprotinin. These observations and our demonstration that enhanced intrarenal activity of the kallikrein-kinin system, consequent to kininase II inhibition, is associated with renal vasodilation, diuresis, and natriuresis, suggest that a coupling of kinins and prostaglandins intrarenally may be directed towards the facilitation of salt-water excretion. The interdigitation of prostaglandins and the kallikrein-kinin system may thereby constitute the essential operation of a regulatory system in which the complementary actions of these hormones antagonize the sodium retaining effect of mineralocorticoids in those states in which salt-water balance is positive.
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PMID:Interaction of mineralocorticoids, renal prostaglandins and the renal kallikrein-kinin system. 76 63

Experiments were conducted on 45 male rats; histophysiological characteristics of ependymocytes of the subcommissural organ (SCO) and of adrencorticocytes of the glomerular zone of the adrenal cortex (GZA) was investigated under conditions of dehydration and water loading. A marked activation of H-6-PDH, HDH, NAD-dependent alphaHPDH, and an enhancement of the H-6-PDH, NAD-diaphorase and 3betaol activity in the GZA adrencorticocytes resulted from dehydration. Water loading depressed the synthetic processes, particularly in the SCO ependymocytes. The data obtained suggest a functional interrelation between the SCO and GZA.
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PMID:[Histophysiological characteristics of the structures of the subcommissural organ of the brain and the glomerular zone of the adrenal gland in changes of the water-electrolyte balance]. 88 35

We have investigated the effective role of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in normal potassium balance in both absence (N3) and presence of E (N3.E). All subjects were submitted to normal dietary intake of sodium (150 mmol/d) and potassium (50 mmol/d). The basal values of PRA, urinary aldosterone and plasma electrolytes were in the normal range. The only significant effect produced by E was a reduction in mean arterial pressure, without significant changes in creatinine cl., urinary hydro-electrolyte excretions as well as urinary excretions of prostanoids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 1) Studies during normal sodium and potassium balance]. 129 5


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