Inotropic responses are also blunted because of downregulation of b 1 -adrenoceptors. Sympathetic activation has other important effects which can be deleterious, including ventricular hypertrophy , enhanced arrhythmogenesis , and molecular and biochemical changes that lead to further dysfunction over time. Therefore, although sympathetic activation may play some compensatory role in the failing heart, there is considerable evidence that it actually exacerbates heart failure. For this reason, the use of beta-blockers in some forms of heart failure has been gaining in popularity because of their proven efficacy. Peripheral vascular constriction Arterial and venous vessels are richly innervated by sympathetic nerves .
Arterial vasoconstriction increases systemic vascular resistance which raises arterial pressure .
In heart failure, particularly when cardiac output is significantly reduced, arterial vasoconstriction helps to maintain arterial pressure. The increased systemic vascular resistance, however, contributes to an increase in afterload on the heart which can further depress systolic function. Peripheral vasoconstriction, particularly in the smaller arterioles, limits muscle perfusion during exercise thereby contributing to the decrease in exercise capacity. Contraction of venous vessels enhance venous return and preload which helps to maintain stroke volume through the Frank-Starling mechanism . The resulting increase in venous pressure, however, can lead to peripheral edema .