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Published on: May 22, 2018
The neurohumoral axis in congestive heart failure
Insights
Congestive heart failure involves increased vasoconstrictor substances like norepinephrine and angiotensin II. New therapies aim to block these vasoconstrictor forces for better heart failure management.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Congestive heart failure (CHF) incidence is rising in the US.
- CHF involves impaired ventricular function and increased vasoconstrictor substances such as norepinephrine, angiotensin II, and arginine vasopressin.
- While compensatory, these systems may contribute to CHF pathogenesis, burdening the myocardium.
Purpose of the Study:
- To explore the role of vasoconstrictor systems in heart failure.
- To review emerging therapeutic strategies targeting vasoconstriction in CHF.
Main Methods:
- Review of existing data on vasoconstrictor system activation in heart failure.
- Analysis of preliminary findings for novel therapeutic interventions.
Main Results:
- Selective blockade of the renin-angiotensin system shows therapeutic utility in CHF.
- Inhibition of the sympathetic nervous system shows potential benefit.
- Vasopressin inhibition is under investigation in animal models of heart failure.
Conclusions:
- Excessive vasoconstriction exacerbates heart failure.
- Targeting vasoconstrictor forces offers promising new therapeutic avenues for CHF.
- Further research into selective blockade of these systems may lead to improved heart failure treatments.
Abstract:
The incidence of congestive heart failure is increasing in the United States. This common syndrome is characterized not only by impaired ventricular function but also by an increase in some endogenous vasoconstrictor substances, including norepinephrine, angiotensin II, and arginine vasopressin. Although activation of the systems that release these substances is presumed to be compensatory (to maintain perfusion pressure during inadequate flow), the sympathetic nervous system, renin-angiotensin-aldosterone system, and arginine vasopressin may contribute to the pathogenesis of the syndrome. The excessive vasoconstriction present in heart failure likely produces a further burden on the failing myocardium. New strategies in therapy are being developed to counteract the activation of vasoconstrictor forces in congestive heart failure. Data indicate that selective blockade of the renin-angiotensin system is useful. Preliminary data suggest that inhibition of the sympathetic nervous system may be helpful, and inhibition of vasopressin in animals with heart failure is being studied. New and more selective therapy for heart failure may come from these studies.
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