O -Adrenergic receptors

Transgenic Models of o -Adrenergic Receptor Subtype Function... 

NIEUWLAND R, WDBtKG OLC, VAN WKLIG01G, AKKHIMAN JWN. o -adrenergic receptors activate proton kinase C in human platdets via a pertussis toxin-sensitive G-piotein.F R5 Rett 339 79-83,1994. 

Localization Based on In Situ or Autoradiography o -Adrenergic Receptors 3.1. Brain... 

Key Words o -Adrenergic receptor blood pressure cardiac cardiovascular hypertrophy knockout. 

Physiological Effects of Altering o -Adrenergic Receptor Gene Expression In Vivo... 

O The lower urinary tract symptoms and signs of benign prostatic hyperplasia are due to static, dynamic, or detrusor factors. The static factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate gland. The dynamic factor refers to excessive stimulation of a-adrenergic receptors in the smooth muscle of the prostate, urethra, and bladder neck. The detrusor factor refers to irritability of hypertrophied detrusor muscle as a result of long-standing bladder outlet obstruction. 

Stevens, D. R., Kuramasu, A., Eriksson, K. S., Selbach, O. Haas, H. L. (2004). Alpha 2-adrenergic receptor-mediated presynaptic inhibition of GABAergic IPSPs in rat histaminergic neurons. Neuropharmacology 46, 1018-22. 

Lefkowitz, R. J., Haber, E., and O Hara, D. (1972). Identification of the cardiac beta-adrenergic receptor protein Solubilization and purification by affinity chromatography. Proc. Natl. Acad. Sci. USA 69, 2828-2832. 

Nikolaev, V. O., Hoffmann, C., Bunemann, M., Lohse, M. J. and Vilardaga, J. P. (2006). Molecular basis of partial agonism at the neurotransmitter alpha2A-adrenergic receptor and Gi-protein heterotrimer. J. Biol. Chem. 281, 24506-11. 

Greasley, P. J., Fanelli, F Rossier, O., Abuin, L., and Cotecchia, S. (2002) Mutagenesis and modelling of the alpha) lb)-adrenergic receptor highlight the role of the helix 3/helix 6 interface in receptor activation. Mol. Pharmacol. 61,1025-1032. 

Figure 5. Schematic of nerve ending and effector cell. 1, liberation of noradrenaline (NA) 2, reuptake 3, combining with a-adrenergic receptor 4, diffusion 5, degradation of NA. MAO = monoamineoxydase, COMT = cat echol-O-methyl-transferase.

The mechanism of action of these drugs is caused by stimulation of o -adrenoreceptors in the inhibitory structure of the brain. It is believed that interaction of these drugs with adrenergic receptors is expressed in the suppression of vasomotor center neurons of the medulla, and reduction of hypothalamus activity, which leads to a decline in sympathetic impulses to the vessels and the heart. In summary, cardiac output and heart rate are moderately reduced, and consequently arterial pressure is reduced. 

Aoki C, Go CG, Venkatesan C, Kurose H (1994) Perikaryal and synaptic localization of OjA-adrenergic receptor-like immunoreactivity. Brain Res 650 181-204 Arnsten AFT, Goldman-Rakic PS (1985) O Adrenergic mechanism in prefrontal cortex associated with cognitive decline in aged nonhuman primates. Science 230 1273-1376... 

Finley JC, O Leary M, Wester D, MacKenzie S, Shepard N, Farrow S, Lockette W. A genetic polymorphism of the alpha2-adrenergic receptor increases autonomic responses to stress. J Appl Physiol 2004 96(6) 2231-9. 

Dopexamine is a synthetic catecholamine with direct and indirect sympathomimetic activity. The indirect effect is caused by potent inhibition of neuronal noradrenaline reuptake. It is a potent 32-adrenoceptor agonist with much less (31- than 32-receptor activity. It also has significant dopaminergic DAl-receptor activity, with only minimal activity at DA2 receptors and no o-adrenergic activity. 

---