Why the study?
Does intravenous infusion of synthetic human CNP-22 stimulate the release of adrenomedullin in healthy subjects?
Does intravenous infusion of synthetic human CNP-22 stimulate the release of adrenomedullin in healthy subjects?
Circulating CNP at pathophysiological levels does not regulate adrenomedullin release, renal hemodynamics, or sodium excretion in healthy humans.
CNP infusion at pathophysiological levels does not affect ADM release or renal hemodynamics in healthy subjects; challenges proposed natriuretic peptide–adrenomedullin crosstalk.
To investigate whether C-type natriuretic peptide (CNP) at pathophysiological plasma levels stimulates the release of adrenomedullin (ADM) in man, six healthy subjects (three men and three women, mean age 35 +/- 3 years, range 33-40 years) received an intravenous infusion of synthetic human CNP-22 (2 pmol kg-1 min for 2 h), in a single-blind, placebo-controlled, random order, cross-over study, with measurements of the plasma levels of cyclic guanosine monophosphate (cGMP), ADM, renin and atrial natriuretic peptide (ANP), arterial pressure, heart rate, renal blood flow (para-aminohippurate clearance), glomerular filtration rate (creatinine clearance), and the urinary excretion rates of cGMP, ADM and sodium. Infusion of CNP induced increases in its own levels (from 1.17 +/- 0.11 up to 21.13 +/- 1.41 pmol l-1) without modifying the plasma levels of cGMP, ADM, renin and ANP, the urinary excretion rate of ADM and cGMP, renal haemodynamics and sodium excretion. These data indicate that circulating CNP is not involved in the regulation of ADM release, renal haemodynamics and sodium excretion in man.
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Lazzeri et al. (1999) studied this question.
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