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Vascular α-Adrenergic Function in Congestive Heart Failure

  • Chapter
Mechanisms of Heart Failure

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 167))

Summary

Congestive heart failure is associated with increased sympathetic nerve activity, which stimulates vascular α-adrenoceptors and modulates systemic vascular resistance. In the early stage of heart failure this may be beneficial in order to maintain adequate systemic pressure and vital organ perfusion. As a result, right and left ventricular filling pressures and pulmonary and systemic vascular resistance are markedly increased, and hepatosplanchnic blood flows are decreased. In the long term, these effects resulting from α-adrenergic stimulation may become detrimental and are associated with deterioration of congestive heart failure. Desensitization or downregulation induced by continuous exposure to a stimulus appears to be a general homeostatic mechanism by which target cells modulate responsiveness to agents acting at the cell’ s surface receptor. In severe congestive heart failure due to prolonged sympathetic stimulation, we have demonstrated that vascular α-adrenoceptors are desensitized and downregulated in a rat model of ischemic heart failure. Furthermore, we have also shown that in patients with severe congestive heart failure, both α1- and α2-adrenoceptor responsiveness is decreased in the dorsal hand veins. The decreased vascular a-adrenergic function may serve as an important mechanism to protect against the excessive vasoconstriction in end-stage heart failure. Although long-term treatment with α1-adrenergic antagonists in patient with congestive heart failure has not been accompanied by an improvement in clinical status, exercise capacity, or survival, further understanding of the α-adrenergic system is important in interpreting neurohumoral and vascular changes in patients with severe heart failure.

Congestive heart failure (CHF) is characterized by increased activity of the sympathetic nervous system. The increased sympathetic tone and neurohormonal activation contribute importantly to vasoconstriction through the activation of vascular α-adrenoceptors in CHF. This vasoconstriction may maintain blood pressure acutely, but chronically the increased afterload will depress cardiac function and contribute to progressive deterioration. The α-adrenergic system plays an important role in the control of vascular resistance. Recently there have been studies on the pathophysiologic changes that may occur in the α-adrenoceptors in patients with CHF. The purpose of this article is to review the physiologic function of the α-adrenergic system and recent developments demonstrating functional changes not only in animal models of CHF but also in patients with CHF.

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  1. Qing-Ping Feng
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  2. J. Malcolm O. Arnold
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  1. MRC Group in Experimental Cardiology Division of Cardiovascular Sciences St. Boniface General Hospital Research Centre Faculty of Medicine, University of Manitoba, Winnipeg, Canada

    Pawan K. Singal , Ian M. C. Dixon , Robert E. Beamish  & Naranjan S. Dhalla , ,  & 

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Feng, QP., Arnold, J.M.O. (1995). Vascular α-Adrenergic Function in Congestive Heart Failure. In: Singal, P.K., Dixon, I.M.C., Beamish, R.E., Dhalla, N.S. (eds) Mechanisms of Heart Failure. Developments in Cardiovascular Medicine, vol 167. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2003-0_4

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