| BAR | bariatrics; barometer, barometric; beta-adrenergic receptor |
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| BARK | beta-adrenergic receptor kinase |
| MBAR | myocardial beta adrenergic receptor |
| ER | efficiency ratio; epigastric region; ejection rate; electroresection; emergency room; endoplasmic re... |
| RAR | rapidly adapting receptor; rat insulin receptor; retinoic acid receptor; right arm reclining; right ... |
| adrenergic neuronal blocking agent | A drug that prevents the release of norepinephrine from sympathetic nerve terminals; it does not inhibit the responses of the adrenergic receptors to circulating epinephrine, norepinephrine, and other adrenergic amines. (05 Mar 2000) |
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| adrenergic uptake inhibitors | Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (antidepressive agents, tricyclic) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin. (12 Dec 1998) |
| alpha-adrenergic blocking agent | An agent that competitively blocks alpha-adrenergic receptors; used in the treatment of hypertension. Synonym: alpha-blocker. (05 Mar 2000) |
| alpha-adrenergic receptors | Adrenergic receptor's in effector tissues capable of selective activation and blockade by drugs; conceptually derived from the ability of certain agents, such as phenoxybenzamine, to block only some adrenergic receptor's and of other agents, such as methoxamine, to activate only the same adrenergic receptor's. Such receptor's are designated as alpha-receptors. Their activation results in physiological responses such as increased peripheral vascular resistance, mydriasis, and contraction of pilomotor muscles. (05 Mar 2000) |
| beta-adrenergic blocking agent | A class of drugs that compete with beta-adrenergic agonists for available receptor sites; some compete for both b1 and b2 receptors (e.g., propranolol) while others are primarily either b1 (e.g., metoprolol) or b2 blockers; used in the treatment of a variety of cardiovascular diseases where beta-adrenergic blockade is desirable. Synonym: beta-adrenergic receptor blocking agent, beta-adrenoreceptor antagonist, beta-blocker. (05 Mar 2000) |
| beta-adrenergic receptors | Adrenergic receptor's in effector tissues capable of selective activation and blockade by drugs; conceptually derived from the ability of certain agents, such as propranolol, to block only some adrenergic receptor's and of other agents, such as isoproterenol, to activate only the same adrenergic receptor's. Such receptor's are designated as beta-receptors. Their activation results in physiological responses such as increases in cardiac rate and force of contraction (b1), and relaxation of bronchial and vascular smooth muscle (b2). (05 Mar 2000) |
| receptors, adrenergic | Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of g-proteins with which they bind; this scheme does not respect the alpha-beta distinction. (12 Dec 1998) |
| receptors, adrenergic, alpha | One of the two major pharmacological subdivisions of adrenergic receptors. The alpha-beta distinction was originally based on cellular effects of receptor activation but now relies on the relative affinities for certain synthetic ligands. Alpha-adrenergic receptors are further subdivided into several subclasses based on studies of endogenous and cloned receptors. (12 Dec 1998) |
| receptors, adrenergic, alpha-1 | A subclass of alpha-adrenergic receptors (receptors, adrenergic, alpha). Alpha-1 adrenergic receptors can be pharmacologically discriminated, e.g., by their high affinity for the agonist phenylephrine and the antagonist prazosin. They are widespread, with clinically important concentrations in the liver, the heart, vascular, intestinal, and genitourinary smooth muscle, and the central and peripheral nervous systems. (12 Dec 1998) |
| receptors, adrenergic, alpha-2 | A subclass of alpha-adrenergic receptors (receptors, adrenergic, alpha). Alpha-2 adrenergic receptors can be pharmacologically discriminated, e.g., by their high affinity for the agonist clonidine and the antagonist yohimbine. They are found on pancreatic beta cells, platelets, and vascular smooth muscle, as well as both pre- and postsynaptically in the central and peripheral nervous systems. (12 Dec 1998) |
| receptors, adrenergic, beta | One of the two major pharmacologically defined classes of adrenergic receptors. The alpha-beta distinction was originally based on the cellular effects of receptor activation but now relies on the relative affinities for characteristic synthetic ligands. Beta adrenergic receptors are further subdivided based on information from endogenous and cloned receptors. (12 Dec 1998) |
| receptors, adrenergic, beta-1 | A subclass of beta-adrenergic receptors (receptors, adrenergic, beta). Beta-1 adrenergic receptors are equally sensitive to epinephrine and norepinephrine and bind the agonist dobutamine and the antagonist metoprolol with high affinity. They are found in the heart, juxtaglomerular cells, and in the central and peripheral nervous systems. (12 Dec 1998) |
| receptors, adrenergic, beta-2 | A subclass of beta-adrenergic receptors (receptors, adrenergic, beta). Beta-2 adrenergic receptors are more sensitive to epinephrine than to norepinephrine and have a high affinity for the agonist terbutaline. They are widespread, with clinically important roles in skeletal muscle, liver, and vascular, bronchial, gastrointestinal, and genitourinary smooth muscle. (12 Dec 1998) |
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
| amino acid receptor | <biochemistry> Ligand gated ion channels with specific receptors for amino acid transmitters. An extended protein superfamily that also includes subunits of the nicotinic acetylcholine receptor. (18 Nov 1997) |