Adrenalin stimulates anion secretion in T84 cells via Ca2+ and cAMP dependent pathway

Short‐circuit current (Isc) technique was used to study the response involved in the electrogenic ion secretion by T84 epithelial cells. Addition of adrenalin to the basolateral membrane of T84 epithelial cells produced a dose‐dependent increase in Isc which consisted of a peak followed by a sustained response considerably higher than the basal Isc.. The EC 50 of adrenalin was about 0.01μM. The transient spike induced by adrenalin could be blocked by phentolamine (non‐specific α‐adrenoceptor antagonist) in a dose‐dependent fashion and the second sustained phase would disappear when T84 epithelial cells were pretreated by propranolol (non‐selective β‐adrenoceptor antagonist, 5μM) on the basolateral side. When the cells were bathed in Cl − ‐free solution, the sustained phase of the Isc upon stimulation with adrenalin was not observed, but the initial spike was still remained. However, these phenomenons were not found when T84 epithelial cells were in HCO 3 − free solution. It suggest that the initial spike was induced by both Cl and HCO 3 − secretion, but the sencond phase of the Isc increase was due to Cl secretion only. Preloading the cells with a cell‐permeant Ca 2+ chelator, BAPTA/AM, abolished the initial spike in the Isc response to adrenalin. On the other hand, the sustained phase was destroyed by pretreating the cells with an adenyl cyclase inhibitor, MDL12330A. These observations suggested that the stimulus‐secretion coupling mechanism might involve Ca 2+ (α‐mediated response) and adenosine cAMP (β‐mediated response) as intracellular second messengers.