Thompson I G, Mills J W
Am J Physiol. 1983 Mar;244(3):C221-6. doi: 10.1152/ajpcell.1983.244.3.C221.
The effects of beta-adrenergic stimulation on the bidirectional fluxes of Na+ and Cl- across the frog skin glands were determined. Isoproterenol elicited net serosal-to-mucosal fluxes of both Na+ (JNanet) and Cl- (JClnet) equal to 0.19 +/- 0.05 (SE) and 0.57 +/- 0.05 mueq X cm-2 X h-1, respectively. The residual current (JClnet - JNanet) of 0.38 +/- 0.05 mueq X cm-2 X h-1 closely approximates the isoproterenol-induced short-circuit current of 0.30 +/- 0.04 mueq X cm-2 X h-1. Furosemide added to the serosal side prior to isoproterenol inhibited the isoproterenol-induced net fluxes of both Na+ and Cl-. The addition of dibutyryl cAMP and 3-isobutyl-1-methylxanthine to the serosal side mimicked the action of isoproterenol by stimulating glandular short-circuit current. We conclude that an active Cl(-)-transport mechanism resides in the frog skin glands and is 1) stimulated by a beta-adrenergic agonist (its action is mimicked by cAMP) and 2) inhibited by the loop diuretic furosemide.
测定了β-肾上腺素能刺激对蛙皮腺中Na⁺和Cl⁻双向通量的影响。异丙肾上腺素引起的Na⁺（JNanet）和Cl⁻（JClnet）从浆膜到黏膜的净通量分别为0.19±0.05（标准误）和0.57±0.05 μeq×cm⁻²×h⁻¹。0.38±0.05 μeq×cm⁻²×h⁻¹的残余电流（JClnet - JNanet）与异丙肾上腺素诱导的0.30±0.04 μeq×cm⁻²×h⁻¹的短路电流非常接近。在异丙肾上腺素之前添加到浆膜侧的呋塞米抑制了异丙肾上腺素诱导的Na⁺和Cl⁻的净通量。向浆膜侧添加二丁酰cAMP和3-异丁基-1-甲基黄嘌呤通过刺激腺体短路电流模拟了异丙肾上腺素的作用。我们得出结论，蛙皮腺中存在一种活跃的Cl⁻转运机制，并且该机制：1）受到β-肾上腺素能激动剂的刺激（其作用可被cAMP模拟）；2）受到袢利尿剂呋塞米的抑制。
