Hypoxic sensitivity in the developing mouse carotid body

It is known that the postnatal development of the hypoxic sensitivity of the carotid body (CB) occurs in the initial 2–3 weeks in several species. The mechanisms of this resetting are still unclear. The question arises at what point postnatally does the mouse CB reset and what factors influence this development. DBA/2J and A/J mice may be useful to investigate the resetting mechanisms, because at 4 to 6 weeks old the hypoxic sensitivity of the CB of A/J mice is minimal compared to the strong response of the DBA/2J mice (carotid sinus nerve activity and changes in intracellular Ca 2+ ([Ca 2+ ]i)). Thus we examined if (1) the gene expression of several K channels and L‐type Ca channels change during development and between strains (RT‐PCR); (2) [Ca 2+ ]i response of the CB develops differently between strains (Fura‐2am). We used 3 age groups: 7, 10 and 14 days old. Of the genes examined, Kcnmb2 (BK β2 subunit) showed a consistently greater expression in the DBA/2J strain compared to the A/J strain. There may be a developmental increase in expression of Kcnma1 (BK α1 subunit) in the DBA/2J mice compared to the A/J mice at 10 days and 2 weeks of age. No significant changes in [Ca 2+ ]i at 7 days old were seen in both strains. The results suggest that BK channel expression may be an important factor for resetting the CB hypoxia response in mice. Supported by AHA 09GRNT2080158, NHLBI HL81345