Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin-converting enzyme (ACE) inhibitors are useful first-line drugs in the therapy of mild and moderate hypertension. Adverse reactions to this drug class are rarely serious. Hypotension, cough, rash, and taste disturbance are uncommon; reduced glomerular filtration and hyperkalemia occur infrequently; angioedema is rare and neutropenia is extremely rare. Quinapril is a new ACE inhibitor that is converted to biologically active quinaprilat in the liver. This ACE inhibitor has a rapid onset of action and inhibits local tissue converting enzyme systems in kidney, heart, and brain, as well as in the circulating renin-angiotensin system. Clinically significant adverse effects of quinapril occur at low rates. In 1,771 patients receiving quinapril, the reported incidence of the first occurrence of orthostatic hypotension was comparable to that seen in patients receiving placebo. In other studies, headache was reported by up to 4.7% of patients receiving quinapril, which is comparable to reported incidences of headache in patients receiving other ACE inhibitors. Other adverse events reported at rates greater than 1% include cough with associated rhinitis and bronchitis, dizziness, and somnolence. Such adverse events have only rarely led to the withdrawal of patients from clinical studies of quinapril.
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PMID:Adverse effects of angiotensin-converting enzyme inhibitors in antihypertensive therapy with focus on quinapril. 154 39

Kininase II (KII), identical with angiotensin-I-converting enzyme (E.C. 3.4.15.1) was characterized biochemically and assayed fluorimetrically in bronchoalveolar lavage fluid and serum of 153 patients with several pulmonary disorders. The albumin concentrations of serum and bronchoalveolar lavage fluid (BLF) have also been measured. The pH optimum of KII derived from BLF (LKII) was 8.0. The Michaelis Menten constant was 38.5 mumol/l using benzyloxycarbonyl-phenylalanyl-histidyl-leucine as synthetic substrate. LKII could be inhibited between 80 and 100% by EDTA, phenanthroline, dimercapto-1-propane-sulfonic acid (DMPS), hydroxyquinoline and captopril. The LKII activity (mU/ml BLF) showed no differences in all lung diseases, but the specific LKII (mU/mg albumin) was significantly elevated in sarcoidosis compared to pneumonia (p less than 0.05), fibrosis (p less than 0.05), chronic obstructive bronchitis (p less than 0.005) and lung cancer (p less than 0.01), but not in tuberculosis. This study shows that LKII is measurable in native, unconcentrated BLF and the results indicate that LKII could be useful for diagnosis of pulmonary disorders.
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PMID:Value of determination of kininase II in bronchoalveolar lavage fluid. 302 72

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