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J Appl Physiol 93: 569-575, 2002. First published April 15, 2002; doi:10.1152/japplphysiol.00027.2002
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Vol. 93, Issue 2, 569-575, August 2002

Hormonal, renal, hemodynamic responses to acute neutral endopeptidase inhibition in heart transplant patients

François Piquard1,2, Ruddy Richard1,2, Anne Charloux1,2, Stephane Doutreleau1,2, Thierry Hannedouche3, Gabrielle Brandenberger1, and Bernard Geny1,2

1 Laboratoire des Régulations Physiologiques et des Rythmes Biologiques chez l'Homme, Equipe d'Accueil 3072, 2 Service de Physiologie et d'Explorations Fonctionnelles, and 3 Service de Néphrologie, Hôpitaux Universitaires et Faculté de Médecine, Université Louis Pasteur, 67085 Strasbourg, France

We investigated the hemodynamic, renal, and hormonal responses to neutral endopeptidase (NEP) inhibition during a 6-h, double-blind, randomized, placebo-controlled study in seven chronic, stable heart transplant patients. Baseline characteristics were similar during both experiments, and no significant changes were observed after placebo. NEP inhibition increased circulating endothelin-1 (from 2.01 ± 0.1 to 2.90 ± 0.2 pmol/l; P < 0.01), atrial natriuretic peptide (ANP; from 21.5 ± 2.7 to 29.6 ± 3.7 pmol/l; P < 0.01), and the ANP second messenger cGMP. Noteworthy, systemic blood pressure did not increase. Renal plasma flow and glomerular filtration rate remained unmodified after NEP inhibition. Filtration fraction (33 ± 13%), diuresis (196 ± 62%), and natriuresis (315 ± 105%) increased significantly in relation to ANP and cGMP. A strong inverse relationship was observed between excreted cGMP and sodium reabsorption (r = -0.71, P < 0.0001). Thus, despite significantly increasing endothelin-1, NEP inhibition did not adversely influence systemic or renal hemodynamics in transplant patients. ANP, possibly through a tubular action, enhances the natriuresis observed after NEP inhibition.

natriuretic peptide; heart transplantation; renal function; cyclosporine; atrial natriuretic peptide


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