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Vasopressin, renin and norepinephrine levels before and after captopril administration in patients with congestive heart failure due to idiopathic dilated cardiomyopathy
Authors:G A Riegger  K Kochsiek
Affiliation:1. School of Nursing, College of Nursing, Taipei Medical University, Taipei, Taiwan;2. Research Center of Biostatistics, School of Nursing, College of Nursing, Taipei Medical University, Taipei, Taiwan;3. School of Gerontology Health Management, College of Nursing, Taipei Medical University, Taipei, Taiwan;4. Post-Baccalaureate Program in Nursing and School of Nursing, College of Nursing, Taipei Medical University, Taipei, Taiwan;5. Master Program in Long-Term Care, College of Nursing, Taipei Medical University, Taipei, Taiwan;6. Department of Health Promotion and Health Education, National Taiwan Normal University, Taipei, Taiwan;1. Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden;2. Heart Failure Unit and Cardiology Service, Hospital Universitari Germans Trias i Pujol, Badalona, Spain;3. Department of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain;4. CIBER Cardiovascular, Instituto de Salud Carlos III, Madrid, Spain;5. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden
Abstract:The effects of 4 weeks of captopril treatment were studied in 10 patients with chronic congestive heart failure (CHF). Acute administration of 50 mg of captopril resulted in an increase in cardiac index and significant decreases in arterial pressure, peripheral vascular resistance and pulmonary capillary wedge pressure. Before treatment, all patients had elevated vasopressin levels (17 +/- 4 pg/ml) relative to decreased plasma osmolality (274 +/- 15 mOsm/kg H2O), and these values were not initially affected by captopril administration (22 +/- 7 pg/ml). However, the relation between arginine vasopressin and plasma osmolality was restored to normal by long-term therapy with captopril (50 mg 3 times daily) (3.0 +/- 1.3 pg/ml; 283 +/- 166 mOsm/kg H2O), which also resulted in sustained improvement of cardiac function. Long-term captopril therapy increased plasma renin concentration from already elevated levels (11 +/- 4 to 32 +/- 8 ng AI/ml X hour) and decreased plasma norepinephrine from 1,054 +/- 244 to 488 +/- 101 pg/ml. Thus, nonosmolar stimulation of vasopressin secretion in CHF can be restored to normal by chronic converting enzyme blockade. The acute vasodilator effects of converting enzyme blockade are not mediated by a reduction of possible vasoconstrictor effects of vasopressin.
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