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Title: Chronic hypercapnia enhances V sub max of Na-H antiporter of renal brush-border membranes

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:5081309

Chronic hypercapnia is associated with increased proximal HCO{sub 3} reabsorption that is thought to be mediated by a Na-H antiporter. The authors hypothesized that chronic hypercapnia would be associated either with increased V{sub max} or with decreased K{sub m} of the Na-H antiporter. To test this hypothesis they made rabbits hypercapnic for 48 h by exposure to 10% CO{sub 2}. In both control and hypercapnic animals, cortical luminal membranes were enriched over the homogenate 16-fold in alkaline phosphatase and 10-fold in maltase activity. The kinetic activity of the Na-H antiporter was measured by the dissipation of the quenching of acridine orange by addition of different Na concentrations. Chronic hypercapnic rabbits had significantly higher V{sub max} of the Na-H antiporter of luminal membranes than controls. The K{sub m}, however, was not different between control and hypercapnic rabbits. {sup 22}Na uptake in presence of an outwardly directed pH gradient was significantly higher in vesicles from hypercapnic rabbits than controls. Amiloride inhibited the Na-H antiporter (as assessed by acridine orange quenching or {sup 22}Na uptake) to the same degree in membranes from both control and hypercapnic rabbits. The uptake of D-({sup 3}H)glucose by luminal membranes was not different between control and hypercapnic rabbits, indicating a specific enhancement of the Na-H antiporter. Thus chronic hypercapnia, but not acute hypercapnia, induces a selective and specific increase in the V{sub max} of Na-H antiporter, and this may mediate the adaptation to chronic hypercapnia.

OSTI ID:
5081309
Journal Information:
American Journal of Physiology; (USA), Vol. 253:3; ISSN 0002-9513
Country of Publication:
United States
Language:
English