Words similar to adrenergic
Example sentences for: adrenergic
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Classical neurotransmitter receptors such as muscarinic acetylcholine receptors (mAChR), adrenergic, dopaminergic, serotoninergic as well as neuropeptide receptors belong to this family ( 1).
The literature surrounding norepinephrine and its role in the development of iron deficient hypertrophy documents the following facts: 1) prolonged iron deficiency causes cardiac hypertrophy [ 11 12 13 14 15 16 17 23 ] , 2) the pool of stored norepinephrine in the heart is decreased with iron deficiency [ 17 21 ] , 3) plasma and urine concentrations of norepinephrine are increased with iron deficiency [ 19 20 21 22 68 ] , and 4) chronic administration of reserpine (which depletes norepinephrine) prevents the development of iron deficient hypertrophy [ 12 ] , but not hypertrophy that results from aortic banding [ 23 ] . This, combined with other studies that relate chronic adrenergic stimulation to hypertrophy, led Rossi to the conclusion that iron deficiency hypertrophy was caused by chronic sympathetic stimulation.
By contrast, a deletion of twelve residues of the human alpha-2A receptor (293-304) which includes the EESSSSE motif did not appear to prevent agonist-induced down-regulation [ 26 ] . Thus a phosphorylation pathway may not be involved in agonist-induced down-regulation of the alpha-2A adrenergic receptor.
Recently, it has been noted that the JNK and p38 pathways can be activated by G-protein coupled receptor agonists, notably angiotensin II, in vascular smooth muscle cells [ 19 20 ] . In cardiac myocytes, both the p38 and JNK pathways have been activated by endothelin-1 (ET-1) and the α 1 adrenergic receptor agonist phenylephrine [ 21 ] . The ability of the JNK and p38 pathways to be activated by the same agonists of G-protein coupled receptors which activate the ERK pathway led to the investigation of 5-HT as a possible activator of the JNK and p38 pathways.
Down-regulation occurs after prolonged agonist treatment (hours to days), resulting in a loss of receptor binding sites [ 2 3 4 ] . The processes involved in homologous desensitization have been extensively investigated for the beta-2 adrenergic receptor, which is the prototypical G protein-coupled receptor.
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