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Alpha-1 adrenergic receptor: Wikis

  

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The alpha-1 (α1) adrenergic receptor is a G protein-coupled receptor (GPCR) associated with the Gq heterotrimeric G-protein. It consists of three highly homologous subtypes, including α1A-, α1B-, and α1D-adrenergic. Catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) signal through the α1-adrenergic receptor in the central and peripheral nervous systems.

Contents

Effects

The α1-adrenergic receptor has several general functions in common with the α2-adrenergic receptor, but also has specific effects of its own.

General

Common (or still unspecified) effects include:

Specific

The primary effect is on smooth muscle, which mainly constrict. However, there are other functions as well.

Smooth muscle

In smooth muscle of blood vessels the principal effect is vasoconstriction. Blood vessels with α1-adrenergic receptors are present in the skin, the sphincters[4] of gastrointestinal system, kidney (renal artery)[5] and brain.[6] During the fight-or-flight response vasoconstriction results in the decreased blood flow to these organs. This accounts for an individual's skin appearing pale when frightened.

It also induces contraction of the urinary bladder[7][8], although this effect is minor compared to the relaxing effect of β2-adrenergic receptors. In other words, the overall effect of sympathetic stimuli on the bladder is relaxation, in order to delay micturition during stress.

Other effects are on smooth muscle are contraction in:

In a few areas the result on smooth muscle is relaxation. These include:

Neuronal

Other

Signaling cascade

α1-Adrenergic receptors are members of the G protein-coupled receptor superfamily. Upon activation, a heterotrimeric G protein, Gq, activates phospholipase C (PLC), which causes an increase in IP3 and calcium. This triggers all other effects. Namely the activation of an enzyme Protein Kinase C. This enzyme being of a kinase nature functions by phosphorylation of other enzymes causing their activation, or by phosphorylation of certain channels leading to the increase or decrease of electrolytes in or out of the cell.

Activity during exercise

During exercise these α1-adrenergic receptors can be selectively blocked by sympathetic nervous activity, allowing the β2-adrenergic receptors (which mediate vasodilation) to dominate. Note that only the α1-adrenergic receptors in active muscle will be blocked. Resting muscle will not have its α1-adrenergic receptors blocked, and hence the overall effect there will be α1-adrenergic mediated vasoconstriction.

Ligands

Various heterocyclic antidepressants and antipsychotics are α1-adrenergic receptor antagonists as well. This action is generally undesirable in such agents and mediates side effects like orthostatic hypotension.

See also

References

  1. ^ Woodman OL, Vatner SF (1987). "Coronary vasoconstriction mediated by α1- and α2-adrenoceptors in conscious dogs". Am. J. Physiol. 253 (2 Pt 2): H388–93. PMID 2887122. http://ajpheart.physiology.org/cgi/content/abstract/253/2/H388. 
  2. ^ Elliott J (1997). "Alpha-adrenoceptkjjkors in equine digital veins: evidence for the presence of both α1 and α2-receptors mediating vasoconstriction". J. Vet. Pharmacol. Ther. 20 (4): 308–17. doi:10.1046/j.1365-2885.1997.00078.x. PMID 9280371. 
  3. ^ Sagrada A, Fargeas MJ, Bueno L (1987). "Involvement of α1 and α2 adrenoceptors in the postlaparotomy intestinal motor disturbances in the rat". Gut 28 (8): 955–9. doi:10.1136/gut.28.8.955. PMID 2889649. 
  4. ^ a b c d Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.  Page 163
  5. ^ Schmitz JM, Graham RM, Sagalowsky A, Pettinger WA (1981). "Renal α1 and α2 adrenergic receptors: biochemical and pharmacological correlations". J. Pharmacol. Exp. Ther. 219 (2): 400–6. PMID 6270306. http://jpet.aspetjournals.org/cgi/content/abstract/219/2/400. 
  6. ^ Circulation & Lung Physiology I M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
  7. ^ a b c d e f g Fitzpatrick, David; Purves, Dale; Augustine, George (2004). "Table 20:2". Neuroscience (Third ed.). Sunderland, Mass: Sinauer. ISBN 0-87893-725-0. 
  8. ^ Chou EC, Capello SA, Levin RM, Longhurst PA (2003). "Excitatory α1-adrenergic receptors predominate over inhibitory β-receptors in rabbit dorsal detrusor". J. Urol. 170 (6 Pt 1): 2503–7. doi:10.1097/01.ju.0000094184.97133.69. PMID 14634460. 
  9. ^ Morton JS, Daly CJ, Jackson VM, McGrath JC (2007). "Alpha1A-adrenoceptors mediate contractions to phenylephrine in rabbit penile arteries". Br. J. Pharmacol. 150 (1): 112–20. doi:10.1038/sj.bjp.0706956. PMID 17115072. 
  10. ^ Cheng JT, Kuo DY (August 2003). "Both alpha1-adrenergic and D(1)-dopaminergic neurotransmissions are involved in phenylpropanolamine-mediated feeding suppression in mice". Neuroscience Letters 347 (2): 136–8. PMID 12873745. http://linkinghub.elsevier.com/retrieve/pii/S0304394003006372. 
  11. ^ a b Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  Page 787

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