Editing Adrenergic receptor (section)

===α receptors===
α receptors have actions in common, but also individual effects. Common (or still receptor unspecified) actions include:
* [[vasoconstriction]]<ref name="pmid9280371">{{cite journal|vauthors=Elliott J|title=Alpha-adrenoceptors in equine digital veins: evidence for the presence of both alpha1 and alpha2-receptors mediating vasoconstriction|journal=Journal of Veterinary Pharmacology and Therapeutics|volume=20|issue=4|pages=308–17|date=1997|pmid=9280371|doi=10.1046/j.1365-2885.1997.00078.x}}</ref>
* decreased flow of [[smooth muscle]] in [[gastrointestinal tract]]<ref name="pmid2889649">{{cite journal|vauthors=Sagrada A, Fargeas MJ, Bueno L|title=Involvement of alpha-1 and alpha-2 adrenoceptors in the postlaparotomy intestinal motor disturbances in the rat|journal=Gut|volume=28|issue=8|pages=955–9|date=1987|pmid=2889649|pmc=1433140|doi=10.1136/gut.28.8.955}}</ref>

Subtype unspecific α agonists (see actions above) can be used to treat [[rhinitis]] (they decrease [[mucus]] secretion). Subtype unspecific α antagonists can be used to treat [[pheochromocytoma]] (they decrease [[vasoconstriction]] caused by norepinephrine).<ref name=":1" />

====α<sub>1</sub> receptor====
{{Main|Alpha-1 adrenergic receptor}}
α<sub>1</sub>-adrenoreceptors are members of the G<sub>q</sub> protein-coupled receptor superfamily. Upon activation, a [[heterotrimeric G protein]], [[Gq alpha subunit|G<sub>q</sub>]], activates [[phospholipase C]] (PLC). The PLC cleaves [[phosphatidylinositol 4,5-bisphosphate]] (PIP<sub>2</sub>), which in turn causes an increase in [[inositol trisphosphate]] (IP<sub>3</sub>) and [[diacylglycerol]] (DAG). The former interacts with [[calcium channel]]s of [[Endoplasmic reticulum|endoplasmic]] and [[sarcoplasmic reticulum]], thus changing the calcium content in a cell. This triggers all other effects, including a prominent slow after depolarizing current (sADP) in neurons.<ref>{{cite journal | vauthors = Smith RS, Weitz CJ, Araneda RC | title = Excitatory actions of noradrenaline and metabotropic glutamate receptor activation in granule cells of the accessory olfactory bulb | journal = Journal of Neurophysiology | volume = 102 | issue = 2 | pages = 1103–14 | date = Aug 2009 | pmid = 19474170 | doi = 10.1152/jn.91093.2008 | pmc=2724365}}</ref>

Actions of the α<sub>1</sub> receptor mainly involve [[smooth muscle]] contraction. It causes [[vasoconstriction]] in many [[blood vessels]], including those of the [[skin]], [[gastrointestinal system]], [[kidney]] ([[renal artery]])<ref name="pmid6270306">{{cite journal|vauthors=Schmitz JM, Graham RM, Sagalowsky A, Pettinger WA |title=Renal alpha-1 and alpha-2 adrenergic receptors: biochemical and pharmacological correlations|journal=The Journal of Pharmacology and Experimental Therapeutics|volume=219|issue=2|pages=400–6|date=1981|pmid=6270306|url=http://jpet.aspetjournals.org/cgi/content/abstract/219/2/400 }}</ref> and [[brain]].<ref>[http://cim.ucdavis.edu/masters/sessions2002/session4_ica.doc Circulation & Lung Physiology I] {{Webarchive|url=https://web.archive.org/web/20110726230145/http://cim.ucdavis.edu/masters/sessions2002/session4_ica.doc |date=2011-07-26 }} M.A.S.T.E.R. Learning Program, UC Davis School of Medicine</ref> Other areas of smooth muscle contraction are:
* [[ureter]]
* [[vas deferens]]
* [[hair]] ([[arrector pili muscle]]s)
* [[uterus]] (when pregnant)
* [[urethral sphincter]]
* [[urothelium]] and [[lamina propria]]<ref name="Moro et al. 2013">{{cite journal|vauthors=Moro C, Tajouri L, Chess-Williams R|title=Adrenoceptor function and expression in bladder urothelium and lamina propria|journal=Urology|volume=81|issue=1|pages=211.e1–7|date=2013|pmid=23200975|doi=10.1016/j.urology.2012.09.011}}</ref>
* [[bronchioles]] (although minor relative to the relaxing effect of β<sub>2</sub> receptor on bronchioles)
* blood vessels of ciliary body and (stimulation  of dilator pupillae muscles of iris causes [[mydriasis]])

Actions also include [[glycogenolysis]] and [[gluconeogenesis]] from [[adipose tissue]] and [[liver]]; secretion from [[sweat gland]]s and [[sodium|Na<sup>+</sup>]] reabsorption from [[kidney]].<ref name=purves/>

[[Α1 antagonist|α<sub>1</sub> antagonists]] can be used to treat:<ref name=":1" />
* [[hypertension]] – decrease blood pressure by decreasing peripheral [[vasoconstriction]]
* [[benign prostate hyperplasia]] – relax [[smooth muscles]] within the prostate thus easing urination

====α<sub>2</sub> receptor====
{{Main|Alpha-2 adrenergic receptor}}
The α<sub>2</sub> receptor couples to the G<sub>i/o</sub> protein.<ref name="pmid18434433">{{cite journal|vauthors=Qin K, Sethi PR, Lambert NA|date=2008|title=Abundance and stability of complexes containing inactive G protein-coupled receptors and G proteins|journal=FASEB Journal|volume=22|issue=8|pages=2920–7|doi=10.1096/fj.08-105775|doi-access=free |pmc=2493464|pmid=18434433}}</ref> It is a presynaptic receptor, causing [[negative feedback]] on, for example, norepinephrine (NE). When NE is released into the synapse, it feeds back on the α<sub>2</sub> receptor, causing less NE release from the presynaptic neuron. This decreases the effect of NE. There are also α<sub>2</sub> receptors on the nerve terminal membrane of the post-synaptic adrenergic neuron.

Actions of the α<sub>2</sub> receptor include:
* decreased [[insulin]] release from the [[pancreas]]<ref name=purves/>
* increased [[glucagon]] release from the pancreas
* contraction of [[sphincter]]s of the [[Gastrointestinal tract|GI-tract]]
* [[negative feedback]] in the neuronal synapses - presynaptic inhibition of norepinephrine release in [[Central nervous system|CNS]]
* increased [[platelet]] aggregation
* decreases peripheral vascular resistance

[[Α2 agonist|α<sub>2</sub> agonists]] (see actions above) can be used to treat:<ref name=":1" />
* [[hypertension]] – decrease blood pressure-raising actions of the [[sympathetic nervous system]]

[[alpha blocker|α<sub>2</sub> antagonists]] can be used to treat:<ref name=":1" />
* [[impotence]] – relax penile smooth muscles and ease blood flow
* [[Depression (mood)|depression]] – enhance mood by increasing [[norepinephrine]] secretion