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Low-dose C-type natriuretic peptide does not affect cardiac and renal function in humans
G Barletta1, C Lazzeri, S Vecchiarino
1Istituto di Clinica Medica e Cardiologia, University of Florence School of Medicine, Italy.
Insights
C-type natriuretic peptide (CNP) infusion in humans did not alter cardiac or renal function, suggesting CNP may not act as a circulating hormone despite its known effects in animals.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Endocrinology
Background:
- C-type natriuretic peptide (CNP) exhibits vasodilating, hypotensive, and natriuretic effects in experimental animals.
- The role of circulating CNP in human cardiac and renal function regulation remains unclear in health and disease.
Purpose of the Study:
- To investigate the effects of systemically administered CNP on cardiac and renal hemodynamics, and hormonal systems in healthy human volunteers.
- To determine if CNP functions as a circulating hormone in humans.
Main Methods:
- A single-blind, placebo-controlled, randomized crossover study involving six healthy volunteers.
- Infusion of CNP at 2 and 4 pmol/kg per minute for 1 hour each.
- Measurements included cardiac and renal hemodynamics, intrarenal sodium handling, plasma/urinary cGMP, renin, and aldosterone levels.
Main Results:
- Plasma CNP levels increased significantly (4- to 10-fold) during infusion, reaching pathophysiological levels.
- No significant changes were observed in cardiac volumes, cardiac output, arterial pressure, renal hemodynamics, or intrarenal sodium handling.
- Plasma and urinary cGMP, renin, and aldosterone levels remained unaffected by CNP infusion.
Conclusions:
- Systemic administration of CNP within the pathophysiological range does not impact systemic hemodynamics, renal function, or the renin-angiotensin-aldosterone system in humans.
- These findings do not support the hypothesis that CNP acts as a circulating hormone in humans.
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.