Neurohormonal interactions and adaptations in congestive heart failure

If vasoconstrictor neurohormones play a detrimental role in the development of congestive heart failure, how can the circulation respond to limit the consequences of this excessive neurohormonal activity? The baroreflex mechanisms that are normally used to control the release of neurohormones are impaired in heart failure. As a result, the circulation must rely on secondary mechanisms - the release of endogenous vasodilators and an alteration in tissue hormonal responsiveness - to maintain homeostasis. Unlike baroreceptor stimulation (which causes a generalized decrease in neurohormonal activity), these secondary mechanisms appear to selectively limit the effects of the vasoconstrictor systems in specific organs. Unfortunately, these adaptive responses become progressively limited in their counterregulatory capacity as heart failure progresses, and thus the vasoconstrictor forces play an increasingly dominant role in the late stages of the disease. This shift in the balance between endogenous and vasodilator hormones appears to be an important determinant of the clinical outcome of these patients. It is likely that most therapeutic interventions in heart failure produce hemodynamic and clinical benefits at least in part by restoring this neurohormonal balance - by interfering with the actions of the vasoconstrictor systems or by potentiating the effects of endogenous vasodilators. Further attempts to modulate the neurohormonal interactions in chronic heart failure will undoubtedly lead to new approaches to the treatment of these severely ill patients.