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Increased Plasma Norepinephrine Levels During Prazosin Therapy for Severe Congestive Heart Failure

WILSON S. COLUCCI, M.D.; GORDON H. WILLIAMS, M.D.; and EUGENE BRAUNWALD, M.D.
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Supported in part by grants HL 16821, HL 1882, and HL 05832 from the National Institutes of Health. Dr. Colucci was supported by training grant HL 07049 from the National Institutes of Health. The studies were done on a Clinical Research Center supported by grant 5-M01-RR00888 from the Division of Research Resources, National Institutes of Health.


Ann Intern Med. 1980;93(3):452-453. doi:10.7326/0003-4819-93-3-452
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Although it is generally agreed that the first administration of prazosin to patients with severe heart failure increases cardiac output and reduces venous pressure by relaxing vascular smooth muscle, there is much controversy over the drug's continued activity during chronic administration. Thus, some investigators have noted rapid tolerance to prazosin's vasodilator action and little or no chronic effectiveness (1, 2), whereas others have found a continued long-term hemodynamic and clinical response to the drug (3, 4). The reason(s) for this wide disparity of findings is unclear but may involve the degree to which various neurohumoral mechanisms are activated (5, 6).

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