Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
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Query: EC:3.1.1.8 (
cholinesterase
)
12,691
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We have studied the effects of various angiotensin-converting enzyme (ACE) inhibitors on intraocular pressure (IOP) of rabbits with experimentally induced
ocular hypertension
and their mechanism of action. Acute
ocular hypertension
was induced by infusion of 5% glucose (15 ml/kg) through marginal ear vein, whereas chronic glaucoma was induced by injection of alpha-chymotrypsin into the posterior chamber of the eye. IOP was measured by tonometer. All ACE inhibitors were instilled topically in the eye in a sterile solution. The effect of ACE inhibitors also was studied on serum
cholinesterase
(true and pseudo) and the enzyme ACE in vitro. Enalaprilat, ramiprilat, and fosinopril produced a time-dependent decrease of IOP in both acute and chronic models of
ocular hypertension
in rabbits. The decrease in IOP was observed for >4 h, and the extent of decrease was comparable to that with both pilocarpine and betaxolol. Prodrugs enalapril and ramipril failed to produced any change in IOP. Losartan also produced a significant decrease in IOP in the chronic model of
ocular hypertension
in rabbits. All the three ACE inhibitors were found to inhibit ACE activity in aqueous humor. The enzyme
cholinesterase
was found to be inhibited by enalaprilat, ramiprilat, and fosinopril. However, atropine did not alter the IOP-lowering effect of enalaprilat in rabbits. Indomethacin pretreatment produced slight but significant inhibition of the IOP-lowering effect of enalaprilat in rabbits. Our data suggest that ACE inhibitors enalaprilat, ramiprilat, and fosinopril produce a significant ocular hypotensive effect in acute and chronic models of
ocular hypertension
in rabbits. Inhibition of ACE in aqueous humor, and in ocular tissues, resulting in reduced angiotensin II formation, could be one of the major mechanisms responsible for the IOP reduction by ACE inhibitors in rabbits.
...
PMID:Oculohypotensive effect of angiotensin-converting enzyme inhibitors in acute and chronic models of glaucoma. 1094 57
We studied the effect of perindopril (1%) on intraocular pressure (IOP) and compared it with the effect of pilocarpine, a therapeutic agent used in experimentally induced acute and chronic models of glaucoma in rabbits. Acute glaucoma was induced by intravenous administration of 5% glucose. Pretreatment with topical perindopril (1%) and pilocarpine (1%) prevented acute rise in IOP induced by intravenous administration of 5% glucose. For inducing chronic
ocular hypertension
in rabbits, 50 units of freshly prepared alpha-chymotrypsin in 0.1 mL of sterile saline was injected in the posterior chamber of the eye. Perindopril (1%) (35 +/- 1.38 mm Hg to 22.45 +/- 1.42 mm Hg) and pilocarpine (1%) (34.4 +/- 0.81 mm Hg to 20.15 +/- 0.69 mm Hg) produced a significant fall in IOP in these rabbits; pretreatment with indomethacin (prostaglandin synthesis inhibitor) did not affect the IOP-lowering action of perindopril (1%). Perindopril (2.71 x 10(-7) mol/L) and neostigmine (1.49 x 10(-7) mol/L) inhibited true cholinesterase and
pseudocholinesterase
enzyme activity in blood. The
cholinesterase
enzyme inhibition by perindopril was comparable with that by neostigmine. In conclusion, our data suggest that perindopril reduced IOP in experimentally induced acute and chronic glaucoma in rabbits. One of the possible mechanisms of perindopril, apart from the inhibition of angiotensin-converting enzyme, may be inhibition of the enzyme
cholinesterase
.
...
PMID:Oculohypotensive effect of perindopril in acute and chronic models of glaucoma in rabbits. 2055 29