AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 5 1204-R1213, Copyright © 1991 by American Physiological Society

ARTICLES

Changes in soluble carbonic anhydrase activity in response to maturation and NH4Cl loading in the rabbit

L. P. Brion, B. J. Zavilowitz, O. Rosen and G. J. Schwartz
Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 10461.

Maturation and systemic acidosis are two factors that stimulate urinary acidification. Proton secretion, CO2 handling, and some metabolic processes are facilitated by cytosolic carbonic anhydrase (CA). The activity of this enzyme in kidney, red blood cells (RBCs), and liver could be regulated in response to acid-base perturbations or maturation. Therefore, we investigated the effects of maturation and NH4Cl acid loading on soluble CA hydratase activity in RBCs, kidneys, and livers of female New Zealand White rabbits during three stages of maturation (neonatal, 4 wk, and adult). Total RBC CA activity doubled with maturation but did not increase after NH4Cl loading. There was substantial interindividual variation in the amount of CA I related activity. In the kidney we found intrinsic cortical CA II activity to be more than twice that in the outer medulla, which was more than twice that in the inner medulla. CA activity doubled with maturation in the cortex and increased by 70% in the outer medulla. Twenty hours after an NH4Cl load there was a 50% increase in renal cortical CA activity in 4-wk-old rabbits, but a comparable increase in cortical CA activity was only seen after 3-5 days of NH4Cl loading in adult animals. In the liver a third of cytosolic CA activity was acetazolamide resistant, presumably CA III, which doubled with maturation. Chronic NH4Cl loading in adult animals induced an almost 60% increase in hepatic acetazolamide-sensitive CA activity (mostly CA II). These data show that in the rabbit there is a renal corticomedullary gradient in soluble CA activity (mostly CA II), with significant activity in the inner medulla. Maturation induced total CA activity in the inner medulla. Maturation induced total CA activity in RBCs, CA II activity in kidney cortex and outer medulla, and CA III in the liver. Finally, CA II activity in kidney cortex and liver appeared to be regulated in response to some conditions of NH4Cl loading.

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