The beta-1 adrenergic receptor is a G-protein-coupled receptor associated with the Gs subunit. This subunit activates adenylate cyclase to activate the cAMP-dependent pathway.
Actions of the beta-1 receptor include increased heart rate in the sinoatrial node. This is known as a chronotropic effect and leads to increased cardiac output in the sympathetic response.
Actions of the beta-1 receptor include increased atrial and ventricular contractility known as an inotropic effect. This leads to increased cardiac output in the sympathetic response.
Activation of this receptor leads to increased renin release from juxtaglomerular cells in the kidney. Renin is an enzyme that breaks down angiotensinogen to angiotensin 1, which is further cleaved by ACE enzyme into angiotensin II. Angiotensin II then constricts blood vessels, increases the secretion of ADH and aldosterone and stimulates the thirst reflex in the hypothalamus, leading to an increase in blood pressure. Therefore, increased renin release plays a role in increased blood pressure in the sympathetic response.
Lipolysis is the breakdown of lipids, which involves the hydrolysis of triglycerides into free fatty acids, which can undergo degradation by beta-oxidation to produce energy for the body. Activation of this receptor can lead to increased lipolysis to help mobilize energy stores during the sympathetic response.
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