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)

The retina, choroid, ciliary body, iris and aqueous humor of swine eyes contain enzymes capable of producing (kallikrein) and inactivating (kininase I and II) kinins. The activity of the enzymes varies in different eye structures. Higher activities of kallikrein and kininase II were found in highly vascularized tissues such as retina, choroid and ciliary body. The highest activity of kininase I (carboxypeptidase N) was found in the aqueous humor. The presence of these enzymes in the eye structures suggests a possible role for them in local metabolism of vasoactive peptides.
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PMID:Kallikrein and kininases in ocular tissues. 299 9

In a study using a stop-flow technique in dog kidney, the existence of kallikrein and kinin was recognized in distal tubules. The presence of kininase I was seen in both distal and proximal tubules, and also partly in the distal tubules. The presence of kininase II in the distal tubules was again confirmed by pretreatment with SQ14225. No evidence of kinin formation, however, was obtained in the proximal nephrons in stop-flow method. From these results, it was suggested that kininase I and II localized in proximal tubules may destroy the kinin filtered from glomeruli at the proximal level, while kallikrein and kininogen and also kininase I and II in the distal tubules may regulate the activity of the renal kallikrein-kinin system in the distal nephrons.
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PMID:Localization of renal kallikrein-kinin system components in the kidney. 301 61

To further clarify the role of the renal kallikrein-kinin system in essential hypertension, a sensitive and simple method for the determination of both human urinary kininase I and kininase II was established, and the system components were determined in patients. In the measurement of kininase activity, desalted urine samples were incubated with synthetic bradykinin, and the reaction was terminated with kininase inhibitors, ethylene diamine tetraacetic acid and phenanthroline. Thus, kininase activity was determined as the kinin-destroying capacity. Moreover, the specific inhibitor for kininase II, SQ14225, was applied for the separation of kininase I and kininase II activities. Daily urinary excretions of total kininase and kininase I activities were significantly higher in essential hypertensive patients than those in normotensive subjects, whereas no difference was observed in kininase II activity. As reported previously, daily excretions of urinary kallikrein and kinin simultaneously determined in these patients were significantly lower than excretions in normotensive subjects. From these results, it was suggested that not only decreased renal kallikrein, but also increased kininase activity, may play an important role in the suppression of the renal kallikrein-kinin system through the reduction of active kinin level in essential hypertension.
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PMID:Urinary excretions of kininase I and kininase II activities in essential hypertension. A sensitive and simple method for its kinin-destroying capacity. 301 73

The paper is concerned with a study of the effect of an excess of corticosteroids in the body, resulting from single and multiple hydrocortisone administration to rats, on the activity of enzymes involved in the pathway of the renin-angiotensin and kinin systems in different parts of the brain and hypophysis. Hydrocortisone administration to rats resulted in an increase in the activity of the angiotensin converting enzyme in the hypothalamus, hippocamp, striate body and hypophysis, an increase in the renin-like activity in the hypothalamus and hippocamp and its decrease in the striate body. The nature of changes in kininase I activity after the hormone administration was different in the examined parts of the brain. The results obtained indicated that one of the links in the mechanism of corticosteroid action on the renin-angiotensin and kinin system of the brain was the effect of these hormones on the activity of the renin-like, angiotensin converting enzymes and kininase I.
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PMID:[Effect of hydrocortisone on the activity of angiotensin-converting and renin-like enzymes and kininase I in the brain and hypophysis of rats]. 302 May 35

Bradykinin (BK) is widely believed to play a role in the pathogenesis of anaphylaxis. To help clarify any such roles, we examined for effects of inhibitors of kininase II (angiotensin converting enzyme, ACE) and "kininase I" (carboxypeptidase N, CPN), on the early course of egg albumin-induced aggregate anaphylaxis in anesthetized guinea pigs. In this model, pulmonary and systemic arterial blood pressure (BP) rise (unless pulmonary fibrillation occurs), lung wgt increases by approximately 60% and pulmonary microvessels are occluded by cell-rich thrombi, all within 5 min of i.v. antigen. The 30 min mortality rate is approximately 2%. ACE inhibitors (BPP9a, Captopril and MK 422; doses up to 140 mumol/kg) do not make anaphylaxis more nor less severe in terms discernible by changes in BP, lung wgt, EKG or intravascular coagulation. In marked contrast, an inhibitor of CPN (2-mercaptomethyl-3-guanidinoethylthiopropionic acid, 2-MGP; 8-16 mumol/kg) increases the 30 min mortality rate to 94% and lung wgt to 180% of control. The animals die in ventricular fibrillation. Given the enormous BK potentiating effects of BPP9a, Captopril and MK 422, it seems likely that little if any BK is formed in the early min of anaphylaxis. 2-MGP does not potentiate BP effects of BK but markedly potentiates effects of C3a anaphylatoxin. Thus, our data support the views that BK is neither a primary nor secondary mediator of aggregate anaphylaxis, and the adverse effects of 2-MGP are best explained in terms of preservation of anaphylatoxins and not in terms of preservation of kinins.
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PMID:Aggregate anaphylaxis and carboxypeptidase N. 302 62

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily urinary excretions of renal K-K system components including kallikrein (KAL), total KAL, pre-KAL, kinin (KIN) and kininase (total, I and II), were measured in 21 normotensives (NT) and 45 patients with EHT (NRH: 29, LRH: 16). Urinary KAL and KIN quantities, KAL activity, total and pre-KAL, and kininase (total, I and II) were measured by direct RIA, kininogenase assay, direct RIA of KAL after trypsin treatment, and KIN destroying capacity, respectively. The daily excretions of KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in EHT than in NT. That of total kininase and kininase I were significantly higher in EHT than in NT while no significant difference was found in kininase I between EHT and NT. In comparing NRH and LRH, the urinary KAL activity and KIN were lower in LRH than in NRH, and kininase I was higher in LRH than in NRH. No significant difference, however, was found in total and pre-KAL, KAL quantity and kininase II between NRH and LRH. The ratio of KAL quantity/total KAL which reflects the conversion rate from pre-KAL in the kidney, did not show any significant difference among NT, NRH and LRH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comprehensive studies on the renal kallikrein-kinin system in essential hypertension. 302 78

In serum of 530 patients with various lung diseases and in 70 healthy control subjects, kininase I (E.C. 3.4.17.3) and kininase II (E.C. 3.4.15.1) were measured spectrophotometrically using hippuryl-L-arginine for estimation of kininase Ia (KIa), hippuryl-L-lysine for kininase Ib (KIb) and hippuryl-L-histidyl-L-leucine for kininase II (KII). KIa and KIb were significantly elevated (p less than 0.02) in lung cancer and sarcoidosis, compared to tuberculosis and healthy controls. There was an increase (p less than 0.05) in lung cancer in relation to sarcoidosis, chronic obstructive bronchitis, tuberculosis, pulmonary fibrosis and healthy control subjects. KII was significantly elevated in sarcoidosis (p less than 0.0001). According to the histological types of lung cancer, no differences of KIa, KIb and KII have been found. The ratio KIa/KIb X KII was 2.3 in lung cancer and 6.7 in the group with sarcoidosis. These results show that the determination of kininases can be used for diagnosis of lung diseases.
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PMID:Kininase I and II activities in serum of patients with lung diseases. 302 81

Some indices of the kallikrein kinin system, namely kininase I (KI), kininase II or angiotensin converting enzyme (KII-ACE) and phenylalanine-arginine aminopeptidase (AP) were analyzed, to detect their levels in ten selected normal subjects and in 20 selected patients with colonic (n = 8) and gastric adenocarcinoma (n = 12). While AP and KI levels did not show differences in the groups under analysis, KII values showed a significant difference (P +/- 0.01), present since the early stages of the diseases and unrelated to the normal laboratory indices.
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PMID:Kininase I, kininase II and aminopeptidase levels in patients with gastrointestinal tumors. 303 83

Carboxypeptidase N (CPN, kininase I) and kininase II (angiotensin converting enzyme) activities were measured simultaneously in blood plasma and synovial fluid in patients suffering from rheumatoid arthritis (RA), psoriatic arthritis (PA) and osteoarthritis (OA) and in the plasma of normal volunteers. CPN levels (defined as the rate of hydrolysis of furylacryloyl-Ala-Lys) in blood were modestly increased and correlated with erythrocyte sedimentation rate in RA and PA. Based on the hydrolysis of synthetic substrates, CPN activity was much higher than kininase II activity in synovial fluid (SF). SF kininase activities were always inferior to the blood levels in all patients and were correlated with the logarithm of SF leukocyte counts, an indicator of the intensity of inflammation. In addition, CPN and albumin levels in SF were highly correlated when expressed as a percent of the plasma concentrations. Biochemical properties of CPN in crude SF confirmed its similarity to blood CPN. Polymorphonuclear leukocytes derived from inflammatory SF did not release CPN. It is concluded that kininases diffuse from the blood into SF through increased vascular permeability and that CPN could be a major metabolic pathway for kinins in this form of exudate. CPN leads to the formation of des-Arg kinins, selective agonists of the B1 receptors for kinins.
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PMID:Carboxypeptidase N (kininase I) activity in blood and synovial fluid from patients with arthritis. 304 Nov 37

A novel method for the synthesis of histargin and its analogs is described. It includes two kinds of N-alkylation reactions that prevent the formation of side products. The inhibition of enzymes by these compounds was also measured. Some of the compounds strongly inhibited carboxypeptidase B, carboxypeptidase A, carboxypeptidase N (kininase I), and angiotensin converting enzyme.
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PMID:Synthesis of histargin and related compounds and their inhibition of enzymes. 320 75


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