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Vasopressin antagonism in heart failure.

Abstract：

:Treatment of chronic heart failure (HF) is based on interference with the renin-angiotensin-aldosterone system and the adrenergic nervous system. Diuretics are used in volume-expanded patients. Insights from clinical trials and registries establish the need to consider correcting both cardiac loading conditions and nonload-related biological factors if HF therapy is to be optimized. Arginine vasopressin (AVP) represents a potentially attractive target for therapy in both acute and chronic HF. Excessive AVP secretion could contribute to both systolic and diastolic wall stress via V1a- and V2-mediated effects on the peripheral vasculature and on water retention. Arginine vasopressin also may directly and adversely affect myocardial function due to the effect of V1a activation on myocardial contractility and cell growth. Last, AVP may contribute to hyponatremia, a powerful predictor of poor outcome in HF. The development of effective nonpeptide antagonists to both the V1a and V2 receptors for AVP now allows for testing the hypotheses that interfering with AVP-mediated signaling could be beneficial in HF. This review summarizes the theoretical rationale for further development of such therapy, reviews the status of current compounds under development, and suggests key issues that need to be addressed as these agents undergo further clinical testing.

journal_name

J Am Coll Cardiol

journal_title

Journal of the American College of Cardiology

authors

Goldsmith SR,Gheorghiade M

doi

10.1016/j.jacc.2005.02.095

subject

Has Abstract

pub_date

2005-11-15 00:00:00

pages

1785-91

issue

10

eissn

0735-1097

issn

1558-3597

pii

S0735-1097(05)01923-6

journal_volume

46

pub_type

杂志文章,评审

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