Effect of α1-adrenergic stimulation of Cl−secretion and signal transduction in exocrine glands (Rana esculenta)

In the present work, the effect of stimulation of α-adrenergic receptors on Cl - secretion via exocrine frog skin glands was investigated. The α-adrenergic stimulation was performed by addition of the adrenergic agonist noradrenaline in the presence of the β-adrenergic antagonist propranolol. In the presence of propranolol, noradrenaline had no effect on the cellular cAMP content. The Cl - secretion was measured as the amiloride-insensitive short circuit current (I SC ). Addition of noradrenaline induced a biphasic increase in the I SC The increase in I SC coincided with an increase in the net 36 Cl - secretion. The noradrenaline-induced increase in I SC was dose-dependent with an EC 50 of 13 ± 0.3 μM. Epifluorescence microscopic measurements of isolated, fura-2-loaded frog skin gland acini were used to characterize the intracellular calcium ([Ca 2+ ] 1 ) response. Application of noradrenaline induced a biphasic [Ca 2+ ] response, which was dose-dependent with an EC 50 of 11 ± 6 μM. The Ca 2+ plateau unlike the peak-response was sensitive to removal of Ca 2+ from the extracellular medium. The noradrenaline-induced increase in the Cl - secretion as well as in [Ca 2+ ] was sensitive to the α 1 -adrenergic antagonist prazosine. Ryanodine and caffeine had no effect on [Ca 2+ ] indicating that the release was independent of ryanodine-sensitive Ca 2+ stores. Noradrenaline mediated a significant increase in the cellular inositol 1,4,5-trisphosphate (IP 3 ) content suggesting that the signal transduction pathway leading to the noradrenaline-induced increase in Ca 2+ involved IP 3 and a release of Ca 2+ from IP 3 -sensitive stores.