Calcium-activated chloride conductance is not increased in pancreatic duct cells of CF mice

Autor: Winpenny, J. P., Verdon, B., McAlroy, H. L., Colledge, W. H., Ratcliff, R., Evans, M. J., Gray, M. A., Argent, B. E.
Zdroj: Pflügers Archiv European Journal of Physiology; May 1995, Vol. 430 Issue: 1 p26-33, 8p
Abstrakt: Calcium-activated anion secretion is elevated in the pancreatic ductal epithelium of transgenic cf/cf mice which lack the cystic fibrosis transmembrane conductance regulator (CFTR). To elucidate whether this effect is due to increased activity of calcium-activated chloride channels, we have studied the relationship between CFTR and calcium-activated chloride currents in pancreatic duct cells isolated from Cambridge cf/cf mice. CFTR chloride currents activated by cAMP were detected in 59% (29/49) of wild-type cells and in 50% (20/40) of heterozygous cells. However, we could not detect any CFTR currents in the homozygous cf/cf cells (0/25). The maximum CFTR current density measured at a membrane potential of 60 mV was 23.5±2.8 pA/pF (n=29) in wild-type cells, and about half that value, i.e. 12.4±1.6 pA/pF (n=20) in heterozygotes (P=0.004). Calcium-activated chloride currents were detected in 73% (24/33) of wild-type, 75% (21/28) of heterozygous and in 58% (7/12) of homozygous cf/cf cells. There was no significant difference between the steady-state calcium-activated current densities in the three genotypic groups; the current measured at 60 mV being 527±162 pA/pF (n=24) from wild-type, 316±35 pA/pF (n=21) from heterozygote and 419±83 pA/pF (n=7) from homozygous cells. Our data suggest that lack of CFTR does not enhance the calcium-activated chloride conductance in murine pancreatic duct cells.
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