inhibitor

1. An agent that restrains or retards physiologic, chemical, or enzymatic action. 2. A nerve, stimulation of which represses activity. SEE ALSO: inhibition.

- α-glucosidase i. an oral agent that aids in the control of diabetes mellitus by delaying the absorption of glucose from the digestive system.α-Glucosidase inhibitors such as acarbose block the function of enzymes produced by mucosal cells of the proximal small bowel that normally break down complex dietary carbohydrates into simple sugars, including glucose. As a consequence, postprandial rises in blood glucose occur much more gradually. Administered before meals, acarbose can reduce peak postprandial glucose levels by as much as 75 mg/dL. Hence it permits reduction in the dose of oral antihyperglycemic agents or insulin. The drug is not absorbed into the circulation and acts only topically on intestinal lining cells. By itself it cannot induce hypoglycemia, but by reducing the need for insulin, it can increase the risk of hypoglycemia for a given dose of a sulfonylurea or insulin. It may cause flatulence, bloating, and diarrhea as complex carbohydrates reach the colon instead of being digested and absorbed.

- angiotensin-converting enzyme inhibitors (ACEI) a class of drugs used in the treatment of hypertension and congestive heart failure; they produce a reduction of peripheral arterial resistance, although the exact mechanism of action has not been fully determined; they block the conversion of angiotensin I to angiotensin II, a powerful vasoconstrictor.

- aromatase inhibitors drugs, such as aminoglutethimide, that inhibit aromatase, an enzyme used in the synthesis of estrogens.

- Bowman-Birk i. a polypeptide that will inhibit both trypsin and chymotrypsin.

- carbonate dehydratase i. an agent, usually chemically related to the sulfonamides, that inhibits the activity of carbonate dehydratase, producing a general decrease in the formation of H₂CO₃ in the tissues. SEE ALSO: acetazolamide, dichlorphenamide. SYN: carbonic anhydrase i..

- carbonic anhydrase i. SYN: carbonate dehydratase i..

- C1 esterase i. an α₂-neuraminoglycoprotein that inhibits the enzymatic activity of C1 esterase, the activated first component of complement. A deficiency of this i. results in a lack of inhibition of C1r and C1s leading to uncontrolled activation of the complement cascade and edema.

- cholinesterase i. a drug, such as neostigmine, which, by inhibiting biodegradation of acetylcholine, restores myoneural function in myasthenia gravis or after nondepolarizing neuromuscular relaxants have been administered.

- familial lipoprotein lipase i. an i. found in certain individuals that inhibits lipoprotein lipase resulting in accumulation of chylomicrons, VLDL, and triacylglycerols; similar in symptoms to familial lipoprotein lipase deficiency.

- glucosidase inhibitors agents such as acarbose that reduce gastrointestinal absorption of carbohydrates. This group of drugs has been known popularly as “starch blockers.” They lower plasma glucose levels and tend to cause weight loss. A limiting side effect is flatulence.

- HMG CoA-reductase inhibitors drugs that interfere with the biosynthesis of cholesterol; used to treat hyperlipidemia.HMG-CoA reductase inhibitors, generically called statins, lower total cholesterol and LDL cholesterol in people with hyperlipidemia, delay progression of atherosclerosis, and decrease the risk of cardiovascular morbidity and mortality. In the synthesis of cholesterol in the liver, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) is converted to mevalonic acid by the enzyme HMG-CoA reductase. Normally this enzyme is inhibited by a high dietary intake of cholesterol, and conversely a reduction of dietary cholesterol may increase HMG-CoA reductase activity. Drugs that block the action of HMG-CoA reductase are structural analogs of HMG-CoA and competitively inhibit the enzyme, preventing cholesterol synthesis. A decline in intracellular cholesterol levels promotes increased expression of cell surface LDL receptors and uptake of circulating LDL. Controlled studies have shown that in people with a history of angina pectoris or heart attack, lovastatin, pravastatin, and simvastatin substantially reduce cardiovascular mortality, conferring protection against unstable angina and lowering the risk of fatal and nonfatal myocardial infarction, the number and duration of hospitalizations, the need for revascularization procedures, and the incidence of transient ischemic attacks and strokes. Prospective studies on the use of these agents by people with normal cholesterol levels have shown substantial reduction in the risk of a major coronary event in postmenopausal women and in people of both sexes over 65. In contrast, studies in which cholesterol was lowered by diet alone or by other drugs ( e.g., cholestyramine, gemfibrozil) have shown no consistent effect on the rate of either heart attacks or strokes. The beneficial effects of cholesterol lowering with statins are independent of concomitant medicines such as aspirin, beta-blockers, and calcium-channel blockers. Hence physical regression of atheroma may not be the principal mechanism by which cholesterol lowering alters cardiac risk. There is experimental evidence that statins affect immune function and the proliferation and metabolism of macrophages and endothelial cells independently of changes in plasma LDL concentrations. Animal studies suggest that statins may reduce the risk of thrombosis after plaque disruption by inhibiting platelet aggregation and maintaining a favorable balance between prothrombotic and fibrinolytic mechanisms. Not all statins have shown equal protective effect. Benefits have been clearly demonstrated only with “natural” statins produced by fermentation (lovastatin, pravastatin, and simvastatin). Synthetic statins have different chemical structures and are metabolized differently; although they lower LDL cholesterol, there are no data to show that they prolong life or reduce the risk of heart attack.

- human α₁-protease i. (α₁PI) SYN: α₁-antitrypsin.

- β-lactamase inhibitors drugs such as clavulanic acid, which are used to inhibit bacterial β-lactamases; often used with a penicillin or cephalosporin to overcome drug resistance.

- lipoprotein-associated coagulation i. (LACI) formerly known as anticonvertin; a protein that inhibits the extrinsic pathway of coagulation by binding to the tissue factor III-factor VII-Ca²⁺-factor Xa complex.

- mechanism-based i. SYN: suicide substrate.

- monoamine oxidase i. (MAOI) a class of chemical compounds that exert antidepressant effect by the reversible or irreversible inhibition of monoamine oxidase A.

- ovulation i. a compound that inhibits ovulation; often found in oral contraceptives.

- protease i. a newly developed class of synthetic drug used in the treatment of HIV infection, with a mode of action different from those of previously used antiretroviral agents including nucleoside analogs.HIV-1 protease activity is critical for the terminal maturation of infectious virions. Protease inhibitors specific for HIV-1 competitively inhibit this enzyme, thereby preventing the maturation of virions capable of infecting other cells. These agents can reduce the viral load (level of HIV RNA in the serum) below the measurable level in a patient with AIDS. Their use has been shown to reduce the risk of disease progression and mortality in patients with HIV infection. They have also been found to improve CD4 counts and reverse AIDS dementia in some patients. Protease inhibitors are administered in combination with nucleoside analogs (nucleoside reverse transcriptase inhibitors) in order to exploit the different modes of action of these 2 classes of antiviral drug. Because emergence of resistance to protease inhibitors has already been a problem, combination regimens including 3 agents are standard. A few strains of HIV have shown resistance to all available protease inhibitors. Significant side effect s of protease inhibitors include elevation of cholesterol and triglyceride levels, insulin resistance and emergence of frank diabetes mellitus, and cosmetically objectionable lipodystrophy (excessive accumulation of fat in the abdomen and breasts accompanied by fat wasting in the face, extremities, and buttocks). Protease inhibitors currently in use include indinavir, nelfinavir, ritonavir, and saquinavir. Several others are in various stages of development and testing.

- proton pump i. agents that block the transport of hydrogen ions into the stomach and hence are useful in the treatment of gastric hyperacidity, as observed in ulcer disease.

- 5α-reductase inhibitors Drugs that inhibit the action of 5α-reductase, resulting in lower levels of prostatic dihydrotestosterone, produced by the enzyme from testosterone as the primary androgen in the prostate.

- residual i. a sound-generating device, worn in the ear, that inhibits or suppresses the sounds of tinnitus by masking, with a residual inhibitory effect when the device is turned off.

- respiratory i. a compound that inhibits the respiratory chain. SYN: respiratory poison.

- selective norepinephrine reuptake i. a class of chemical compounds that selectively, to varying degrees, inhibit the reuptake of norepinephrine by the presynaptic neurons and are posited to exert their antidepressant effect by this mechanism.

- selective serotonin reuptake i. a class of chemical compounds that selectively, to varying degrees, inhibit the reuptake of serotonin by presynaptic neurons and are posited to exert their antidepressant effect by this mechanism.

- serine protease inhibitors a class of highly polymorphic inhibitors of trypsin, elastase, and certain other proteases synthesized by hepatocytes and macrophages SEE ALSO: α₁-antitrypsin. SYN: serpins.

- serotonin norepinephrine reuptake i. a class of antidepressant drugs whose action is thought to result from inhibition of presynaptic reuptake of serotonin and norepinephrine.

- suicide i. SYN: suicide substrate.

- trypsin i. 1. a peptide formed from trypsinogen via hydrolysis under the catalytic influence of enteropeptidase, with trypsin also produced as a result; so called because the peptide masks or inhibits the active site of the trypsin molecule; 2. one of the polypeptides, from various sources ( e.g., human and bovine colostrum, soybeans, egg white), that inhibit the action of trypsin. Cf.:Bowman-Birk i..

- α₁-trypsin i. SYN: α₁-antitrypsin.

- uncompetitive i. a type of enzyme i. in which the inhibiting compound only binds to the enzyme-substrate complex.

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in·hib·i·tor in-'hib-ət-ər n one that inhibits: as

a) an agent that slows or interferes with a chemical reaction

b) a substance that reduces the activity of another substance (as an enzyme)

c) a gene that checks the normal effect of another nonallelic gene when both are present

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n.

a substance that prevents the occurrence of a given process or reaction. See also MAO inhibitor.

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in·hib·i·tor (in-hibґĭ-tər) 1. any substance that interferes with a chemical reaction, growth, or other biological activity. 2. a chemical substance that inhibits an enzyme reaction. See also inhibition.