Abstract
Three studies were performed: (1) a controlled investigation of α-human atrial natriuretic peptide (α-hANP) total body production and metabolic clearance rates using a bolus infusion technique (controls, patients 1 to 6); (2) a study of α-hANP kinetics in cardiac dysfunction patients using a constant infusion method (patients 7 to 14); and (3) a right heart catheterization study to determine the amount of α-hANP released into the circulation at the level of the right heart, estimated by the step-up in α-hANP concentration between the superior and inferior vena cava and the pulmonary artery, in the patients with left ventricular dysfunction. Baseline venous plasma α-hANP was 27.3 ± 16.5 pg/ml in the controls (mean ± SD; N = 6), 141.6 ± 138.0 pg/ml in patients 1 to 6 (P < 0.05 compared to controls), and 167.5 ± 145.7 pg/ml in patients 7 to 14. Total body α-hANP production rate was markedly elevated in patients 1 to 6 compared to controls (0.45 ± 0.36 vs. 0.11 ± 0.06 μg/min, P < 0.05) and was similar to that determined by the continuous infusion technique in patients 7 to 14 (0.62 ± 0.44 μg/min, P = 0.49 compared to patients 1 to 6). α-hANP release into the right heart (0.17 ± 0.11 μg/min), however, was significantly lower than total body production rate in the cardiac dysfunction patients, indicating that total body α-hANP secretion occurs from sites in addition to drainage into the right heart via the coronary sinus and anterior cardiac veins. Right atrial pressure correlated with the α-hANP released into the right heart. We conclude that in our patients with left ventricular dysfunction, increased α-hANP productiion was the major factor contributing to the elevated plasma α-hANP concentrations; moreover, considerable amounts of α-hANP were also secreted into the circulation at sites other than the right heart.
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CITATION STYLE
Hensen, J., Abraham, W. T., Lesnefsky, E. J., Levenson, B., Groves, B. M., Schroder, K., … Durr, J. (1992). Atrial natriuretic peptide kinetic studies in patients with cardiac dysfunction. Kidney International, 41(5), 1333–1339. https://doi.org/10.1038/ki.1992.197
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