Adrenergic Receptor

Adrenergic Receptor

Adrenergic receptors are a class of G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine and epinephrine. Many cells possess these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system. The sympathetic nervous system is responsible for the fight-or-flight response, which includes widening the pupils of the eye, mobilizing energy, and diverting blood flow from non-essential organs to skeletal muscle.

Adrenergic receptors (ARs) are a family of G protein-coupled receptors (GPCRs) that are activated by the endogenous catecholamines NE and Epi. Epi and NE are important in the stress response and influence a diverse range of physiological processes. This is possible in part to the diversity of AR subtypes expressed on different mammalian tissues. Nine AR subtypes, α1A-, α1B-, α1D-, α2A-, α2B-, α2C-, β1-, β2-, and β3- have been characterized and their effects on cardiac output, smooth muscle and metabolic process have been extensively studied. Changes in an animal's susceptibility and ability to fight infection during times of stress have been documented however, AR expression and function in the immune system is not well characterized. Furthermore, during any injuiy or infection, catecholamines will be release and could be influencing the healing process. Like glucocorticoids, another product of the stress response, ARs have historically been thought to be anti-inflammatory and immunosuppressive. However, dichotomous effects of NE on immune cell populations and during disease states suggest that AR mechanisms in the .

Adrenergic receptors are so termed because of their response to norepinephrine or epinephrine. Alpha, beta, and dopaminergic adrenergic receptors have been identified. Alpha 1 receptors are located in the smooth muscle of the coronary vasculature, as well as in the heart, skin, uterus, intestinal mucosa, and splanchnic beds. Activation of alpha 1 receptors results in constriction of the coronary beds, increased inotropy in the heart, and relaxation of the intestinal tract. Alpha 2 postsynaptic receptors mediate peripheral arterial and venous vasoconstriction, platelet aggregation, inhibition of insulin release, and inhibition of ADH release. Alpha 2 presynaptic receptors mediate the negative norepinephrine feedback loop, and therefore increase circulating levels of norepinephrine.

Beta adrenergic receptors are divided into the subtypes beta 1, beta 2, and beta 3. Beta 1 receptors are located in the myocardium, sinoatrial node, and ventricular conduction system, and therefore can alter the inotropy and chronotropy of the heart. Beta 1 receptors also impact the release of renin from the juxtaglomerular apparatus in the kidney. This release of renin enhances angiotensin II production, leading to vasoconstriction in the renal efferent arterioles. Antidiuretic hormone and aldosterone release is also increased, as is sodium reabsorption form the proximal tubule. These mechanisms lead to renal cortical vasoconstriction, decreases in glomerular filtration rate, and both sodium and water retention. Beta 2 receptors are located in the myocardium, the vasculature smooth muscle and in the pulmonary system. Beta 2 receptors are more sensitive to epinephrine than norepinephrine and mediate the chronotropic response of the heart, as well as vasodilatation of the vasculature, bronchial relaxation, and a vasodilatory response in the kidneys. Beta 3 receptors play a role in modulating energy metabolism and thermogenesis. These receptors are located in the adipose tissue and the gastrointestinal tract and are thought to be coupled to lipolysis in human adipocytes. Through the various beta receptors, a wide array of systemic functions are maintained and able to be promptly altered.

Laurel A. Grisanti. ADRENERGIC RECEPTOR MODULATION OF LJPOPOLYSACCHARTDE-MEDIATED INFLAMMATORY RESPONSES

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