Kudo K, Kondo Y, Abe K, Igarashi Y, Tada K, Yoshinaga K
Department of Clinical Biology and Hormonal Regulation, Tohoku University School of Medicine, Sendai, Japan.
Am J Physiol. 1991 Sep;261(3 Pt 2):F393-9. doi: 10.1152/ajprenal.1991.261.3.F393.
The effect of isoproterenol on the electrophysiological properties of the S2 proximal segment of the rabbit was examined. Isoproterenol at 10(-8) to 10(-4) M depolarized the basolateral membrane voltage (Vb) in a dose-dependent manner. Propranolol attenuated the isoproterenol-induced depolarization. These possible mechanisms of cell depolarization were explored. The role of luminal Na(+)-organic solute cotransport was negligible, since the removal of organic solute did not change the depolarization. Basolateral Na(+)-(HCO3-) cotransport was supported by the finding that 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibited isoproterenol-induced depolarization. Basolateral K+ conductance was suggested by the finding that the application of Ba2+ blocked the isoproterenol-induced depolarization. Na(+)-K(+)-adenosine-triphosphatase (ATPase) was questionable. Although ouabain blocked isoproterenol-induced depolarization, the removal of Na+ did not inhibit the depolarization. Further experiment revealed that dibutylyl-adenosine 3',5'-cyclic monophosphate (cAMP), 8-bromo cAMP, and forskolin did not mimic the response of isoproterenol. These results demonstrate: 1) there is a functional beta-adrenoceptor that depolarizes Vb; 2) isoproterenol-induced depolarization is due to an inhibition of basolateral K+ channel or the activation of basolateral Na(+)-(HCO3-)n cotransport; 3) isoproteronol-induced depolarization is independent of cAMP in the rabbit proximal tubule.
研究了异丙肾上腺素对兔S2近端节段电生理特性的影响。10(-8)至10(-4)M的异丙肾上腺素以剂量依赖方式使基底外侧膜电压（Vb）去极化。普萘洛尔减弱了异丙肾上腺素诱导的去极化。探讨了细胞去极化的这些可能机制。由于去除有机溶质并未改变去极化，因此管腔Na(+)-有机溶质共转运的作用可忽略不计。4,4'-二异硫氰基芪-2,2'-二磺酸抑制异丙肾上腺素诱导的去极化这一发现支持了基底外侧Na(+)-(HCO3-)共转运。应用Ba2+阻断异丙肾上腺素诱导的去极化这一发现提示了基底外侧K+电导。Na(+)-K(+)-腺苷三磷酸酶（ATPase）存在疑问。虽然哇巴因阻断了异丙肾上腺素诱导的去极化，但去除Na+并未抑制去极化。进一步的实验表明，二丁酰腺苷3',5'-环一磷酸（cAMP）、8-溴cAMP和福斯可林并未模拟异丙肾上腺素的反应。这些结果表明：1）存在一个使Vb去极化的功能性β-肾上腺素能受体；2）异丙肾上腺素诱导的去极化是由于基底外侧K+通道的抑制或基底外侧Na(+)-(HCO3-)n共转运的激活；3）在兔近端小管中，异丙肾上腺素诱导的去极化与cAMP无关。
