Adrenergic receptors
Pharmacological effects of adrenergic drugs are mediated by activation of adrenergic receptors. Two types of adrenergic receptors were proposed to explain the dissimilar effects of sympathomimetic agents in different tissues. They are α and β receptors.
The α and β receptors are differentiated pharmacologically, initially based on the relative properties of catecholamines namely epinephrine, norepinephrine and isoproterenol.
Effects of adrenoceptors
Released catecholamines interact with the α-adrenergic or β-adrenergic receptors on the postjunctional membrane to produce specific effects in the postjunctional cell through activation of specific G-proteins.
In some systems released catecholamines interact with a α2 -adrenergic receptors, which are on the prejunctional nerve cell. These receptors mediate an inhibition of the release of norepinephrine thus allowing the neurotransmitter to modulate its own release. This has been termed as auto-inhibitory feedback mechanism and may play an important role in the regulation of catecholamine release.
In general, α receptors mediate excitatory/contractile response and β receptors mediate stimulation of the heart, relaxation of smooth muscles and metabolic effects.
In addition to these receptors, dopamine receptors are available in periphery, which mediate vasodilatation in the kidney, heart, mesentry and increase the force of contraction of the heart. Dopamine also has a weak agonistic activity on the α adrenergic receptors.
Adrenergic receptors and adrenergic responses
| α actions | β actions |
| Constriction of arterioles and veins – rise in BP | Dilatation of arterioles and veins – fall in BP |
| Heart – little action, arrhythmia in high doses | Cardiac stimulation, increased heart rate, force and conduction velocity |
| – | Bronchodilatation |
| Contraction of radial muscles of the eye – mydriasis, decreased aqueous secretion | No effect on iris and ciliary muscles, enhanced aqueous secretion |
| Intestinal relaxation, contraction of sphincters | Intestinal relaxation |
| Bladder trigone – contraction | Detrusor – relaxation |
| Uterus – contraction | Relaxation |
| Splenic capsule – contraction | Relaxation |
| Neuromuscular transmission facilitated – increased Ach | Active state – prolonged in fast contracting muscle, abbreviated in slow contracting muscle |
| Insulin secretion inhibited ( œ2 dominant) | Augmented insulin (mild) |
| Liver – glycogenolysis | – |
| – | Renin release from the kidney |
| Male sex organs – ejaculation | – |
| Salivary glands – K+ and H2O secretion | Ptylin secretion |
| – | ADH secretion from posterior pituitary |
| Nictitating membrane – contraction in some species | – |
Subtypes of α adrenoceptors
| * | α1 | α2 |
| Location | Postjunctional effector organs | Prejunctional nerve ending, postjunctional in brain, pancreatic β cells, platelets and extrajunctional in blood vessels |
| Function subserved | Smooth muscle – contractionBlood vessels -VasoconstrictionGlands – decreased secretionGut – relaxationHeart – arrhythmia | Inhibitors of transmitter releaseBlood vessels-VasoconstrictionDecreased central sympathetic flowDecreased insulin releasePlatelet aggregation |
| Selective agonist | Phenylephrine, methoxamine | Clonidine |
| Selective antagonist | Prazosin | Yohimbine |
Subtypes of β adrenoceptors
| * | β1 | β2 | β3 |
| Location and function subserved | Heart – increased heart rate, increased force of contraction, increased AV nodal conduction velocityJuxtaglomerular cells in kidney – increased renin secretion | Bronchi – relaxationBlood vessels – VasodilatationUterus – relaxationGI tract – relaxationUrinary tract – relaxationSkeletal muscle – glycogenolysisLiver – glycogenolysis | Adipose tissue – lipolysis |
| Selective agonist | Dobutamine | Salbutamol | – |
| Selective antagonist | Atenolol | Butoxamine | – |
