Figure 9.

Proposed cell model for cAMP/PKA-mediated Cl- secretion by SCCD epithelium. Cl- is taken up across the basolateral membrane by NKCC (Na+-K+-2Cl- cotransporter). A Na+-K+-ATPase and Ba2+-sensitive K+ conductance in the basolateral membrane is thought to create a negative cell membrane potential that drives Cl- exit across the apical membrane via a Cl- channel, likely CFTR. Cl- secretion is stimulated by PKA from activation of a basolateral β2-adrenergic receptor (β2-AR; activated by agonists such as isoproterenol, ISO) coupled to a cAMP second messenger pathway (Gs-protein activation of adenylyl cyclase (AC) which can also be directly activated by forskolin (FSK). Phosphodiesterase (PDE) catabolizes cAMP and can be inhibited by IBMX and RO-20-1720 (RO-20). The cAMP-dependent Cl- secretion pathway is further stimulated by activation of intracellular glucocorticoid receptors (not shown) after chronic exposure to glucocorticosteroids.

Pondugula et al. BMC Physiology 2013 13:6   doi:10.1186/1472-6793-13-6
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