Atriopeptin turnover: quantitative relationship between in vivo changes in plasma levels and atrial content.
Administration of the 1-deamino-arginine8 vasopressin caused a decrease in right, but not left, atrial levels of atriopeptin (AP) in chloral hydrate-anesthetized rats. The amount of exogenous AP required to match the 1-deamino-arginine8 vasopressin-stimulated plasma levels of AP was equivalent to the decrease in AP content of the right atrium, suggesting that resynthesis of AP did not occur within the 60 min after 1-deamino-arginine8 vasopressin stimulation. The correlation between increased plasma levels and decreased atrial content was also observed in bilaterally nephrectomized rats, suggesting that the kidney is not a major site of degradation of AP in vivo. This finding was confirmed by the comparison of the half-life of exogenous AP in normal (T1/2 = 31 sec) and nephrectomized (T1/2 = 64 sec) animals. Plasma immunoreactivity of the N-terminal fragment of the prohormone (which is also released after cleavage of the precursor peptide) increased 35-fold by 24 hr after nephrectomy in comparison with a 5-fold increase in AP. Half-life studies of the N-terminal fragment suggest that the kidney is the major site of degradation of this molecule. This study demonstrated the different kinetics and renal metabolism of the AP and N-terminal portions of the prohormone.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism*; D003894:Deamino Arginine Vasopressin / Q000031:analogs & derivatives / Q000494:pharmacology; D006207:Half-Life; D006325:Heart Atria / Q000378:metabolism; D007700:Kinetics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009392:Nephrectomy; D010446:Peptide Fragments / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D010446:Peptide Fragments; C025161:vasopressin, deamino-homo-Arg-; D009320:Atrial Natriuretic Factor; D003894:Deamino Arginine Vasopressin