The Adrenergic Receptors

The Adrenergic Receptors

The term adrenergic originally referred to the effects of epinephrine (adrenaline), as opposed to the cholinergic effects of acetylcholine. Norepinephrine (noradrenalin) is the neurotransmitter responsible for most of the adrenergic activity of the sympathetic nervous system. Adrenergic receptors are divided into two general categories alpha (α) and (β). Each of these has been further subdivided into at least two subtypes: α1 and α2, and β1 and β 2.

  • Alpha-1 receptors: α1-Receptors are postsynaptic adrenoceptors located in smooth muscle throughout the body, in the eye, lung, blood vessels, uterus, gut, and genitourinary system. They are associated with mydriasis (pupillary dilation due to contraction of the radial eye muscles), bronchoconstriction, vasoconstriction, uterine contracture, and contraction of sphincters in the gastrointestinal and genitourinary tracts. The most important cardiovascular effect of α1-stimulation is vasoconstriction, which increases peripheral vascular resistance, left ventricular after load, and arterial blood pressure.
  • Alpha-2 receptors: α 2-receptors create a negative feedback loop that inhibits further norepinephrine release from the neuron. Stimulation of postsynaptic α 2-receptors in the central nervous system causes sedation and reduces sympathetic outflow, which leads to peripheral vasodilation and lower blood pressure.
  • Beta-1 receptor: The most important β 1-receptors are located on postsynaptic membranes in the heart. Stimulation of these receptors has positive chronotropic (increased heart rate), dromotropic (increased conduction), and inotropic (increased contractility) effects.
  • Beta-2 receptor: β 2-Receptors are primarily postsynaptic adrenoceptors located in smooth muscle and gland cells. . Despite this commonality, β 2-stimulation relaxes smooth muscle, resulting in bronchodilation, vasodilation, and relaxation of the uterus (tocolysis), bladder, and gut. Glycogenolysis, lipolysis, gluconeogenesis, and insulin release are stimulated by β 2 receptor activation. β 2-Agonists also activate the sodium-potassium pump, which drives potassium intracellularly and can induce hypokalemia and dysrhythmias.

Last modified: Wednesday, 16 November 2016, 4:02 PM