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 ³⁶Cl^? secretion. The noradrenaline‐induced increase in I_SC was dose‐dependent with an EC₅₀ of 13 ± 0.3 μM . Epifluorescence microscopic measurements of isolated, fura‐2‐loaded frog skin gland acini were used to characterize the intracellular calcium (Ca²⁺]_i) response. Application of noradrenaline induced a biphasic Ca²⁺]_i response, which was dose‐dependent with an EC₅₀ of 11 ± 6 μM . The Ca²⁺ plateau unlike the peak‐response was sensitive to removal of Ca²⁺ from the extracellular medium. The noradrenaline‐induced increase in the Cl^? secretion as well as in Ca²⁺]_i was sensitive to the α₁‐adrenergic antagonist prazosine. Ryanodine and caffeine had no effect on Ca²⁺]_i indicating that the release was independent of ryanodine‐sensitive Ca²⁺ stores. Noradrenaline mediated a significant increase in the cellular inositol 1,4,5‐trisphosphate (IP₃) content suggesting that the signal transduction pathway leading to the noradrenaline‐induced increase in Ca²⁺ involved IP₃ and a release of Ca²⁺ from IP₃‐sensitive stores.