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The expression of acid‐base transporters in the neonatal and adult mouse exposed to chronic hypercapnia
Author(s) -
Kanaan Amjad,
Douglas Robert M,
Kelly Michelle L,
Alper Seth L,
Boron Walter F,
Haddad Gabriel G
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1283-c
Subject(s) - hypercapnia , intracellular ph , homeostasis , transporter , sodium–hydrogen antiporter , medicine , antiporter , endocrinology , acidosis , kidney , chemistry , base excess , metabolic acidosis , sodium , intracellular , biochemistry , gene , organic chemistry
Several disease conditions result in hypercapnia and disturbance in pH homeostasis. We hypothesize that exposure to chronic hypercapnia will induce changes in the expression of membrane acid‐base transporter (ABT) proteins. Neonatal and adult CD‐1 mice were exposed to either 8% or 12% CO2 for 2 weeks. We used western blot analysis of membrane proteins from various brain regions, heart, and kidney to study the response of sodium hydrogen exchangers NHEs, sodium bicarbonate co‐transporter NBCs, and anion exchangers AEs to CO2. In neonates, 8% CO2 increased the expression of NHE1 in the cerebral cortex and heart by 25% and 55% respectively, and increased NBCn1 in cortex and heart by 30%, and also increased AE3 expression in the heart by 50% (p<0.05). In adults, 8% CO2 had no effect on ABT expression. In neonates, 12% CO2 increased NHE1 in cortex, heart and kidney by 30%, 66%, and 64% respectively, and increased NBCn1 in cortex, heart and kidney by 57%, 70% and 50% respectively (p<0.05). 12% CO2 significantly decreased the expression of AE3 in both the neonatal and adult brain by 40% and 40–70% respectively. Conclusions: Chronic hypercapnia increases the expression of the acid extruders NHE1 and NBCn1 and decreases that of the acid loader AE3, improving tissue acid‐extruding capacity. There is heterogeneity in the response of tissues to hypercapnia that is also dependent on the level of CO2 and development.