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Relationship between plasma atriopeptin concentration and function in the conscious primate

C Hoegler, J McIntyre, G Zeballos, J Shapiro, M DeLeonardis, P Needleman and T Hintze

Department of Physiology, New York Medical College, Valhalla.

The renal actions of atriopeptins (APs) 24, 21 and 28 were examined in the conscious primate, macaca fascicularis. AP-24 increased urine flow rate and sodium excretion 20- and 100-fold, respectively. The circulating form of the atriopeptins, AP-28, had similar, even slightly greater (25%) effects when compared to AP-24. AP-21 on the other hand had dramatically reduced effects, less than 20%, when compared to either AP-24 or AP-28. Infusion of AP-24 resulted in marked increases in plasma immunoreactive AP and in renal function. There were direct, significant linear relations between plasma levels and arterial pressure, heart rate, glomerular flow rate, urine flow rate, sodium and potassium excretion. However, the threshold for these effects was generally higher than expected, i.e., greater than 100 pg/ml. Interestingly, there was a 4-fold greater slope for sodium excretion when compared to other renal functions implying a distinctly different mechanism of action. Whereas, the plasma half-life of the peptide was 2 to 3 min, the biological half-life varied from 6 min for sodium excretion to 10 min for urine flow and potassium excretion. The increased slope for the relationship between sodium excretion and plasma AP concentration and the short half-life for sodium excretion indicate that the change in renal sodium handling is independent of urine flow rate and glomerular filtration rate. There is a direct and linear relationship between plasma peptides and renal function which may imply a cause and effect relationship. This extrapolation may, however, be valid only when plasma peptide levels are elevated markedly.

Volume 251, Issue 3, pp. 929-936, 12/01/1989
Copyright © 1989 by American Society for Pharmacology and Experimental Therapeutics




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[Abstract] [Full Text]


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Copyright © 1989 by the American Society for Pharmacology and Experimental Therapeutics.