Changes

===='''''Response to stimulus'''''====

===='''''Response to stimulus'''''====

Adrenaline released from the adrenal medulla into the circulation, and noradrenaline released at nerve terminals, stimulates cardiac and vascular '''beta and alpha-receptors''', resulting in increased contractility of the heart (beta-receptors) and vasoconstriction of both the arterial and venous side of the circulation (alpha-receptors).

Adrenaline released from the adrenal medulla into the circulation, and noradrenaline released at nerve terminals, stimulates cardiac and vascular '''alpha and beta-receptors''', resulting in vasoconstriction of both the arterial and venous side of the circulation (alpha-receptors) and increased contractility of the heart (beta-receptors).

'''Beta Effects''':

'''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.

Stimulation of beta-receptors leads to stimulation 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 a positive inotrope (increased myocardial contractility which increases cardiac output), positive chronotrope (increased heart rate), and positive luisitrope (improved diastolic relaxation) effect, and stimulates renin release from the [[Reabsorption_and_Secretion_Along_the_Distal_Tubule_and_Collecting_Duct_-_Anatomy_%26_Physiology#Juxtaglomerular_Apparatus|Juxtaglomerular apparatus (JGA)]].

''advantages'':

'''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)]].

Increased strength of cardiac contraction; increased rate of cardiac contraction and improved myocardial relaxation.

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.

 

Increased myocardial oxygen consumption (increased heart rate and increased work due to inotropic stimulation); 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.

 

 

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.

'''NOTE''' There is a strong correlation between the severity of heart failure and the degree of stimulation of the adrenergic system. Veterinary studies have confirmed greater stimulation of the adrenergic system in patients with more advanced heart disease. Human studies have demonstrated a worse prognosis in those patients with higher levels of circulating noradrenaline.

'''NOTE''' There is a strong correlation between the severity of heart failure and the degree of stimulation of the adrenergic system. Veterinary studies have confirmed greater stimulation of the adrenergic system in patients with more advanced heart disease. Human studies have demonstrated a worse prognosis in those patients with higher levels of circulating noradrenaline.