Beta 1 Receptors

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Alhayek S, Preuss CV

Beta 1 Receptors

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Abstract

Beta-1 receptors, along with beta-2, alpha-1, and alpha-2 receptors, are adrenergic receptors primarily responsible for signaling in the sympathetic nervous system. Beta-agonists bind to the beta receptors on various tissues throughout the body. Beta-1 receptors are predominantly found in three locations: the heart, the kidney, and the fat cells. The beta-1 adrenergic receptor is a G-protein-coupled receptor communicating through the Gs alpha subunit. By signaling Gs, a cAMP-dependent pathway is initiated through adenylyl cyclase, and this results in potentiation of the receptor's function. Targeted activation of the beta-1 receptor in the heart increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility. With these two increased values, the stroke volume and cardiac output will also increase. This effect clearly shows in the cardiac output equation. Cardiac output equals the product of stroke volume and heart rate. As either stroke volume or heart rate increase, both of which will increase with targeted activation of the beta-1 receptor, cardiac output will increase, thus increasing perfusion to tissues throughout the body. In the kidney, smooth muscle cells in the juxtaglomerular apparatus contract and release renin. This cascading effect will eventually increase blood volume through the actions of angiotensin II and aldosterone. In the adipocyte[1], the beta-1 receptor is targeted to upregulate lipolysis. Various hormones may target the adrenoreceptors with different affinities. In this article, we will focus on the beta receptors, in particular, beta-1 adrenergic receptors. The chemicals epinephrine, dopamine, and isoproterenol[2] target beta-1 and beta-2 receptors almost equally. Norepinephrine and dobutamine target beta-1 to a greater degree than beta-2. While hormones are the normal pathway by which these systems typically activate, they can also be activated or blocked medically through a multitude of pharmacologic therapies, some of which will be discussed below.

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Drugs: Pindolol