Atrial natriuretic peptide inhibits renal glutamine extraction.
The effect of administered atrial natriuretic peptide, ANP, on renal glutamine extraction, oxygen consumption and ammoniagenesis was determined in the intact functioning kidney of nonacidotic and chronically acidotic rats. Chronic acidosis shifted the metabolic fuel dependency towards glutamine, reflected by a 3.7 fold increase in extraction. Bolus injection of ANP, 1 microgram/100g BW, results in increased GFR, massive diuresis and an acid urine. Glutamine uptake fell in both groups, reversing from uptake to release in nonacidotic animals and dropping nearly 50 percent in acidotic rats. In contrast, oxygen consumption fell only 20 percent. Inhibition of glutamine extraction appears to be an indirect effect of ANP dependent upon the elevated GFR and elimination of glutamine uptake from the blood, but not from the filtrate. Efficacy of ANP, unlike classical diuretics, was not affected by the prevailing acid base condition nor a large shift in the fuel utilized.
Welbourne
T C
TC
Department of Physiology and Biophysics, LSUMC, Shreveport.
Solomon
S
S
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D004231:Diuresis / Q000187:drug effects; D005971:Glutamates / Q000097:blood; D005973:Glutamine / Q000037:antagonists & inhibitors* / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects; D007668:Kidney / Q000378:metabolism* / Q000502:physiology; D008297:Male; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism
D005971:Glutamates; D005973:Glutamine; D009320:Atrial Natriuretic Factor; D012964:Sodium