Changes

'''Alpha Effects''' increase arterial blood pressure and protects perfusion of essential vascular beds (cerebral and coronary) but the increased systemic vascular resistance leads to increased afterload and decreased cardiac output, with increased myocardial oxygen demand. It is likely to exacerbate hypoperfusion of non-essential vascular beds.

'''Alpha Effects''' increase arterial blood pressure and protects perfusion of essential vascular beds (cerebral and coronary) but the increased systemic vascular resistance leads to increased afterload and decreased cardiac output, with increased myocardial oxygen demand. It is likely to exacerbate hypoperfusion of non-essential vascular beds.

'''Beta Effects''' stimulate the release of adenylate cyclase, which generates intracellular cyclic AMP. This in turn has many intracellular effects, including increasing the rate and magnitude of the contractions in intracellular calcium fibres. This has positive inotrope (increased myocardial contractility which increases cardiac output), positive chronotrope (increased heart rate), and positive luisitrope (improved diastolic relaxation) effects, and stimulates renin release from the [[Reabsorption_and_Secretion_Along_the_Distal_Tubule_and_Collecting_Duct_-_Anatomy_%26_Physiology#Juxtaglomerular_Apparatus|Juxtaglomerular apparatus (JGA)]].

'''Beta Effects''' stimulate the release of adenylate cyclase, which generates intracellular cyclic AMP. This in turn has many intracellular effects, including increasing the rate and magnitude of the contractions in intracellular calcium fibres. This has positive inotrope (increased myocardial contractility which increases cardiac output), positive chronotrope (increased heart rate), and positive luisitrope (improved diastolic relaxation) effects, and stimulates renin release from the [[Reabsorption_and_Secretion_Along_the_Distal_Tubule_and_Collecting_Duct_- Anatomy & Physiology#Juxtaglomerular_Apparatus|Juxtaglomerular apparatus (JGA)]].

These effects lead to an increased rate and strength of cardiac contraction, and improved myocardial relaxation. This process does, however increase myocardial oxygen consumption (increased heart rate and increased work due to inotropic stimulation) and increased intracellular calcium can lead to calcium overload that in turn can result in cardiac rhythm disturbances and cell death. Chronic stimulation leads to down-regulation of the system.

These effects lead to an increased rate and strength of cardiac contraction, and improved myocardial relaxation. This process does, however increase myocardial oxygen consumption (increased heart rate and increased work due to inotropic stimulation) and increased intracellular calcium can lead to calcium overload that in turn can result in cardiac rhythm disturbances and cell death. Chronic stimulation leads to down-regulation of the system.