Neurohormonal activation in congestive heart failure and the role of vasopressin
Neurohormonal activation in congestive heart failure and the role of vasopressin
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DOI：
10.1016/j.amjcard.2005.03.003
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发表时间：
2005-05-02
影响因子：
2.8
通讯作者：
Chatterjee, K
中科院分区：
文献类型：
--
作者：
Chatterjee, K
血管活性神经激素系统（例如，交感神经系统[SNS]、肾素-血管紧张素-醛固酮系统和精氨酸加压素[AVP]）是旨在在低心输出量期间保持动脉容量和循环稳态的防御机制。神经激素系统通常在急性血容量不足的情况下受到刺激，并被低心输出量和动脉压激活。然而，这些系统的持续和慢性激活，如充血性心力衰竭（CHF）中发生的情况，可能会导致进行性心室重塑和心力衰竭恶化。血管收缩、水潴留和血容量增加是 SNS、肾素-血管紧张素途径和 AVP 分泌激活的结果。这些影响会加速 CHF 的进展，导致发病率和死亡率增加。 AVP 分别通过加压素 V-1a 和 V-2 受体亚型调节血管张力和自由水重吸收，因此是治疗 CHF 的潜在神经激素靶点。 (c) 2005 年，Excerpta Medica Inc.
Vasoactive neurohormonal systems (eg, sympathetic nervous system [SNS], renin-angiotensin-aldosterone system, and arginine vasopressin [AVP]) are defense mechanisms designed to preserve arterial volume and circulatory homeostasis during periods of low cardiac output. Neurohormonal systems, which are normally stimulated under conditions of acute volume depletion, are activated by the low cardiac output and arterial pressure. However, sustained and chronic activation of these systems, as occurs in congestive heart failure (CHF), can cause progressive ventricular remodeling and worsening heart failure. Vasoconstriction, water retention, and increased blood volume are results of the activation of the SNS, the renin-angiotensin pathway, and AVP secretion. These effects can accelerate progression of CHF, contributing to increased morbidity and mortality. AVP regulates vascular tone and free-water reabsorption, respectively, through the vasopressin V-1a and V-2 receptor subtypes and therefore is a potential neurohormonal target in the treatment of CHF. (c) 2005 by Excerpta Medica Inc.