700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ ReadersThis Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
Patients with cystic fibrosis demonstrate a defect in HCO3 - secretion by their pancreatic duct cells. However, attempts toward understanding or correcting this defect have been hampered by a lack of knowledge regarding the cellular and molecular mechanisms mediating HCO3 - transport in these cells. Recent functional and molecular studies indicate a major role for a basolateral electrogenically-driven Na+ :HCO3 - cotransporter (NBC1) in mediating the transport of HCO3 - into the duct cells. The HCO3 - exits at the lumen predominantly via two recently discovered apical HCO3 - transporters. cAMP, which mediates the stimulatory effect of secretin on pancreatic ductal HCO3 - secretion, potentiates the basolateral Na+ :HCO3 - cotransporter due to generation of a favorable electrogenic gradient as a result of membrane depolarization by Cl- - secreting cystic fibrosis transmembrane conductance regulator (CFTR). Two apical HCO3 - transporters drive the secretion of bicarbonate into the pancreatic duct lumen. Molecular and functional studies indicate that CFTR upregulates the expression of these two apical HCO3 - transporters. In addition, CFTR may also upregulate the expression of certain water channels and facilitate the secretion of fluid into the duct lumen. In brief, current research suggests that the defect in pancreatic HCO3 - secretion in patients with cystic fibrosis is multifactorial and involves the alteration in the function/expression of transporters at the basolateral and luminal membrane domains of the duct cells.