Receptor human adrenergic

Green SA, Turki J, Innis M, Liggett SB. Amino-terminal polymorphisms of the human -adrenergic receptor impart distinct agonist-promoted regulatory properties. Biochemistry 1994 33 9414-9419. 

Small, K. M., Mcgraw, D. W., and Liggett, S. B. (2003) Pharmacology and physiology of human adrenergic receptor polymorphisms. Annu. Rev. Pharmacol. Toxicol. 43, 381M11. 

De Vos H, Bricca G, De Keyser J, et al Imidazoline receptors, non-adrenergic idazoxan binding sites and a2-adrenoceptors in the human central nervous system. Neuroscience 59 589-598, 1994... 

Haske, T.N. DeBlasi, A. LeVine, H. An intact N terminus of the y subunit is required for the G/ly stimulation of rhodopsin phosphorylation by human -adrenergic receptor kinase-1 but not for kinase binding. J. Biol. Chem., 271, 2941-2948 (1996)... 

Many physiological functions have been linked to specific subtypes of ar, o -, and (3-adrenergic receptors in various animal species. Because of the obvious reason of limited access, particularly regarding healthy tissue, similar progress for human adrenergic receptors has been slower and in many cases limited to the characterization of expression of RNA for the receptor subtypes. A more extensive characterization of protein and function for all the human adrenergic receptor subtypes is needed to identify specific targets for possible therapeutic intervention. 

Eason MG, Liggett SB. Human -adrenergic receptor subtype distribution widespread and subtype-selective expression of a2C10, a2C4, and a2C2 mRNA in multiple tissues. Mol Pharmacol 1993 44 70-75. 

Rathz DA, Brown KM, Kramer LA, Liggett SB. Amino acid 49 polymorphisms of the human -adrenergic receptor affect agonist-promoted trafficking. J Car-diovasc Pharmacol 2002 39 155-160. 

Pharmacology and Physiology of Human Adrenergic Receptor Polymorphisms... 

Figu re 1 Localization of nonsynony mous polymorphisms of human adrenergic receptors. Shown is a prototypic adrenergic receptor and the approximate location of amino acid substitutions or deletions. 

PHARMACOLOGY AND PHYSIOLOGY OF HUMAN ADRENERGIC RECEPTOR POLYMORPHISMS... 

Characterization of the allosteric interactions between antagonists and amiloride at the human ajA-adrenergic receptor. Mol. Pharmacol. 53 916-925. 

Studies have now started to clarify the role of histamine Hi and H2 receptors in the cardiovascular manifestations of anaphylaxis. However, histamine can activate H3 and H4 receptors [56, 57]. Levi and coworkers [58-60] identified H3 receptors as inhibitory heteroreceptors in cardiac adrenergic nerve endings. This suggests a mechanism by which endogenous histamine can activate norepinephrine release in normal and ischemic conditions [61,62]. The functional identification ofH3 receptors in the human heart [59] means that these receptors might be directly and/or indirectly involved in the cardiovascular manifestations of anaphylactic reactions. 

Epinephrine and norepinephrine have equal affinity for Pj-receptors, the predominant adrenergic receptors on the heart. However, the human heart also contains a small percentage of P2-receptors that, like Pj-receptors, are excitatory. Therefore, epinephrine is capable of stimulating a greater number of receptors and causing a greater stimulatory effect on the myocardium. 

The major circulating hormones that influence vascular smooth muscle tone are the catecholamines epinephrine and norepinephrine. These hormones are released from the adrenal medulla in response to sympathetic nervous stimulation. In humans, 80% of catecholamine secretion is epinephrine and 20% is norepinephrine. Stimulation of cy-adrenergic receptors causes vasoconstriction. The selective a,-adrenergic receptor antagonist, prazosin, is effective in management of hypertension because it causes arterial and venous smooth muscle to relax. 

M, Ligett SB. A polymorphism of the human /f adrenergic receptor within the fourth transmembrane domain alters ligand binding and functional properties of the receptor. J Biol Chem 1993 268 23116-23121. 

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