Vasopressin Antagonism in Heart Failure

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Vasopressin antagonism in heart failure.

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 va...

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Vasopressin antagonism: a future treatment option in heart failure.

Arginine vasopressin plays an important role in volume homeostasis. Patients with heart failure have chronically elevated plasma vasopressin concentrations which may contribute to their clinical syndrome of fluid retention. Recently, a number of agents have been developed to antagonize the effects of vasopressin by targeting its V1a and V2 receptors, which are involved in vascular tone and free...

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Aldosterone antagonism in heart failure

Aldosterone, a neurohormone known to affect electrolytes, has recently been implicated as playing a major role in the progression of heart failure, particularly in patients with systolic dysfunction. Major clinical trials designed to analyze clinical outcomes using an aldosterone antagonist have been done in two groups with heart failure. The first was the Randomized Aldactone Evaluation Study,...

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Arginine vasopressin in heart failure.

Pathogenesis of AVP Release In several animal models of low-output and high-output cardiac failure and in congestive heart failure in humans, it has been demonstrated that plasma AVP, renin activity, aldosterone and norepinephrine are significantly increased.7 Renal excretion of sodium and water is predominantly regulated by the integrity of the arterial circulation, which is determined by card...

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Selective V2-receptor vasopressin antagonism decreases urinary aquaporin-2 excretion in patients with chronic heart failure.

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ژورنال

عنوان ژورنال: Journal of the American College of Cardiology

سال: 2005

ISSN: 0735-1097

DOI: 10.1016/j.jacc.2005.02.095