Low-Dose C-Type Natriuretic Peptide Does Not Affect Cardiac and Renal Function in Humans

Author:

Barletta Giuseppe1,Lazzeri Chiara1,Vecchiarino Sabrina1,Del Bene Riccarda1,Messeri Gianni1,Dello Sbarba Antonio1,Mannelli Massimo1,La Villa Giorgio1

Affiliation:

1. From the Istituto di Medicina Interna (C.L., S.V., A.D.S., G.L.V.), Istituto di Clinica Medica e Cardiologia (G.B., R.D.B.), Dipartimento di Fisiopatologia Clinica (M.M.), Unità di Endocrinologia, University of Florence School of Medicine, and Laboratorio di Endocrinologia (G.M.), Azienda Ospedaliera Careggi, Florence, Italy.

Abstract

Abstract —In experimental animals, C-type natriuretic peptide (CNP) has vasodilating, hypotensive, and natriuretic activities. The role of circulating CNP in the overall regulation of cardiac and renal function in humans is less defined, in both health and disease. We measured cardiac volumes, diastolic and systolic functions, systemic (Doppler echocardiography) and renal hemodynamics, intrarenal sodium handling (lithium clearance method), plasma and urinary cGMP, plasma renin concentration, and plasma aldosterone level in six healthy volunteers (mean age, 33±3 years) receiving CNP (2 and 4 pmol/kg per minute for 1 hour each) in a single-blind, placebo-controlled, random-order, crossover study. During CNP infusion, plasma CNP increased from 1.17±0.23 to 41.52±4.61 pmol/L (ie, 4- to 10-fold higher levels than those observed in disease states) without affecting plasma and urinary cGMP, cardiac volumes, dynamics of left and right heart filling, cardiac output, arterial pressure, renal hemodynamics, intrarenal sodium handling, sodium excretion, or plasma levels of renin and aldosterone. The finding that increments in plasma CNP within the pathophysiological range have no effects on systemic hemodynamics, renal function, or the renin-angiotensin system do not support the hypothesis that CNP may act as a circulating hormone in humans.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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