A. Beta-1-adrenergic receptors regulate heart rate and myocardial contractility, but in situations of stress with the provocation of epinephrine release stimulation of cardiac beta-2 receptors contribute to additional increases in heart rate and contractility.

β-Adrenergic receptors (βARs) control key physiological functions by transducing signals encoded in catecholamine hormones and neurotransmitters to activate intracellular signaling pathways. We also discuss the spectacular insights into adrenergic receptor function that were obtained from the structures.

βARs are activated by endogenous catecholamines epinephrine/norepinephrine and binding of these receptors on cardiomyocytes results in positive inotropic and chronotropic responses. Agonist binding to βAR results in a conformational change leading to receptor coupling to Gsα subtype of hetero-trimeric G protein.

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.

Beta-2 adrenoceptors are activated by the catecholamines norepinephrine and epinephrine, and are members of the adrenoceptor family of the 7-transmembrane superfamily of receptors.

Beta-2 agonists are drugs that selectively mimic the actions of the endogenous catecholamines epinephrine and norepinephrine. As pharmaceuticals, their major role is to reduce signs and symptoms of asthma and chronic obstructive pulmonary disease by bronchodilation, allowing the patient to breathe more easily.

The beta-2 adrenergic receptor (β2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-adrenergic receptor that binds epinephrine (adrenaline), a hormone and neurotransmitter whose signaling, via adenylate cyclase stimulation through trimeric Gs proteins, increased cAMP, and downstream L-type calcium …

Beta-1 receptors are located in the heart. When beta-1 receptors are stimulated they increase the heart rate and increase the heart’s strength of contraction or contractility. The beta-2 receptors are located in the bronchioles of the lungs and the arteries of the skeletal muscles. Increased cardiac contractility.

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.

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.

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.

The beta-1 adrenergic receptor, the dominant receptor in heart and adipose tissue, is equally sensitive to epinephrine and norepinephrine, whereas the beta-2 adrenergic receptor, responsible for relaxation of vascular, uterine, and airway smooth muscle, is less sensitive to norepinephrine as compared to epinephrine.