Sympathetic activity and regional blood flow in heart failure

The syndrome of heart failure results from inappropriate sodium and water retention by the kidneys which results, at least in part, from changes in renal haemodynamics. Renal blood flow at rest in heart failure is reduced in proportion to the reduction in cardiac output and falls dramatically during exercise as the cardiac output is redistributed to the exercising muscles. Both these phenomena are associated with a rise in plasma noradrenaline concentration. Afferent arteriolar tone is partly controlled by alpha-adrenoceptor stimulation while stimulation of beta 2-receptors will stimulate renal release of renin; through the elaboration of angiotensin II, profound effects on extra- and intra-renal vascular tone can occur. Although alpha-adrenoceptor stimulation can result in coronary vasoconstriction and a fall in coronary blood flow in patients with heart failure due to underlying atheromatous coronary heart disease, increased myocardial oxygen demand as the result of beta 1 (and cardiac beta 2) simulation may be more relevant. The control of limb blood flow is of great importance symptomatically. The systemic vasoconstriction that typifies the severe heart failure state has been a target for many vasodilatory interventions including alpha 1-receptor blockade and beta 2-receptor stimulation. Unfortunately, there is little evidence that such treatment leads to any specific increase in muscle blood flow either at rest or during exercise. In severe heart failure, sympathetic activity is increased at rest leading to vasoconstriction in several vascular beds, while in milder heart failure, excessive sympathetic stimulation is evident only during exercise. In either circumstance, however, it is evident that certain advantages may accrue from modulation of this excessive sympathetic activity.