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Receptors of the Body

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by

Yi Yang

on 5 February 2014

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Transcript of Receptors of the Body

Adrenergic Receptors
Beta Receptors
Alpha Receptors
Activated by catecholamines such as norepinephrine and epineprine
GPCRs
Alpha-1
- located post-synaptically in the vascular smooth muscle, genitourinary tract, and the eye.
Alpha-2
- autoreceptors on the neural pre-synaptic membrane and pancreatic beta cells. Inhibit NE release.
Beta-1
- located in the heart and kidneys.
Beta-2
- located in the bronchial muscle, uterine muscle, ciliary eye, liver, bladder detruser muscle, and vascular smooth muscle.
Beta-3
- located in adipose tissue.
Receptors of the Body
By: Yi Yang
PharmD. Candidate
Muscarinic Receptors
Acetylcholine

GPCRs
M1
- autonomic ganglia, salivary glands, and stomach.
M2
- heart, GI tract, bladder detruser muscle.
M3
- salivary glands, bladder detruser muscle, GI tract, eye.
M4
- autonomic ganglia.
M5
- sphincter muscle of eye, esophagus, parotid gland.
Activation causes vasoconstriction leading to increased peripheral vascular resistance and hypertension.
Alpha-1 Receptor- Vascular Smooth Muscle
Alpha-1 antagonists act as peripheral dilators to decrease blood pressure.
Alpha-1

and

Alpha-2

Receptors- Eye
Activation causes mydriasis by constriction of the radial muscle of the iris.
Activation causes miosis by constriction of the iris sphincter muscle.
M3

and

M5

Receptors-
Eye
Affects both arterioles and veins.
Alpha-2 Receptor- Salivary Glands
Constriction of smooth muscles in the salivary glands inhibits salivation.
Alpha-2 Receptors- Stomach and Intestines
Activation leads to decreased motility and tone

Contraction of sphincters (usually)
Activation causes contraction of the internal and external urethral sphincter muscles causing urinary continence.
Alpha-1A Receptors- Bladder
Alpha-1A antagonists block these actions to promote voiding.
So many receptors!
Hmm, a visual review of
systems would be nice...
Constriction of blood vessels in the eye. Treatment of ophthalmic hyperemia.
Alpha-1 Receptors- Nasal Mucosa
Constriction of blood vessels in nasal mucosa relieves nasal congestion.
Alpha-1 Receptor- Heart
Alpha-1 Receptors do not directly affect the heart.
Alpha-1 mediated vasoconstriction increases blood pressure and can activate the baroreceptor reflex. Result is decreased heart rate and possible bradycardia.
Alpha-2 Receptor- CNS
Alpha-2 agonism in the CNS reduces sympathetic outflows to the heart and cardiovascular system. Result is lowering of blood pressure.
Activation can also lead to relief of severe pain.
Alpha-2 Receptor- Heart and Vasculature
Alpha-2 antagonism leads to increased release of NE.
Increased beta-1 effects on the heart and increased alpha-1 effects on the vasculature.
Beta-1 Receptor- Heart
Activation leads to a positive inotropic effect. Increased force of contraction and cardiac output.
Activation leads to a positive chronotropic effect. Increased heart rate and possibly tachycardia.
Enhanced conduction through AV node. Possibly overcoming AV block.
Beta-2 Receptor- Lungs
Activation causes bronchodilation. Can help prevent/relieve asthma attacks.
Beta-1 Receptor- Kidneys
Activation of beta-1 receptors on juxtaglomerular cells stimulate renin release.
Renin release can cause vasoconstriction through the renin-angiotensin pathway.
Inhaled beta agonists decrease systemic effects.
Activation causes relaxation of uterine smooth muscle. Can be used to delay premature labor.
Beta-2 Receptor- Uterus
Beta-2 Receptors- Liver
Activation promotes the breakdown of glycogen into glucose in the liver and skeletal muscles.
Can be problematic for diabetic patients.
M2 and M3 Receptors- Bladder
Activation causes direct contraction of the bladder detrusor muscle causing mituration urge.
3:1 ratio in favor of M2 receptors.
Antagonism of these receptors leads to decrease in urinary urgency.
M1 and M3 Receptors- Salivary Glands
Activation causes production of saliva in salivary and parotid glands.
Antagonism of these receptors reduce salivation and can cause dry mouth.
M2 and M3 Receptors- GI Tract
Activation is required for contraction of gastrointestinal smooth muscles and motility.
Antagonism of these receptors will cause decreased motility and constipation depending on severity.
Beta antagonism can lead to bronchoconstriction and cause bronchospams.
M1 and M3 Receptors- Lungs
Activation causes contraction of airway smooth muscle and bronchoconstriction.
Receptors in the airway epithelium and submucosal glands facilitate mucus secretion.
Antagonism of these receptors causes bronchodilation and decreased mucus production.
M2 Receptor- Lungs
M2 receptors serve as inhibitory prejunctional autoreceptors in the lungs.
M2 antagonism can cause an increase in acetylcholine release resulting in bronchoconstriction.
M2 Receptor- Heart
Stimulation will decrease heart rate through pacemaker modulation, decrease conduction velocity in AV node, and force of contraction of atrial muscle.
M2 antagonism will increase sympathetic activity in the heart and cause tachycardia.
Beta-3 Receptor- Adipose Tissue
Involved in lipolysis and thermogenesis.
Effects of antagonism are unknown.
Agonism of alpha-2 receptors decrease aqueous humor production and increase uveoscleral outflow. Result is decreased intraocular pressure.
Antagonism causes mydriasis with loss of accommodation.
Beta-1 and Beta-2 Receptors- Eye
Antagonism causes decreased aqueous humor production, increased outflow, and decreased intraocular pressure.
Beta agonism can increase intraocular pressure.
Any Questions?
Alpha-2 Receptor- Pancreas
Inhibits insulin release.
Stimulates glucagon release.
Full transcript