Joris L, Quinton P M
Division of Biomedical Sciences, University of California, Riverside 92521-0121.
Am J Physiol. 1991 Jun;260(6 Pt 1):L510-5. doi: 10.1152/ajplung.1991.260.6.L510.
Basic components of unstimulated electrolyte transport across equine tracheal mucosa were characterized. After the tissue was mounted in Ussing chambers, both current and tissue resistance gradually increased for approximately 60 min before reaching stable values. Thereafter, under open-circuit conditions, the tissue had a resistance of 250 +/- 14 omega.cm2, generated a transepithelial potential difference of -34 +/- 1.7 (SE) mV (referenced to the serosal side) and an equivalent short-circuit current (Ieqsc) of -149 +/- 10.2 microA/cm2. Even though 10(-5) M amiloride reduced the current by approximately 65%, mucosal Na+ substitution with choline decreased the current significantly more (approximately 80%), indicating that part of the Na(+)-dependent current was amiloride insensitive. No current decrease occurred after serosal application of 10(-4) M bumetanide, which was expected to inhibit Na(+)-K(+)-2Cl(-)-mediated Cl- secretion, even though bilateral Cl- substitution with gluconate reduced Ieqsc by approximately 30 microA/cm2. Continuous short-circuit conditions caused a reversible fall in the short-circuit current that was inhibited by amiloride but not by Cl- depletion, suggesting that sustained short circuiting leads to a significant underestimation of the amiloride-sensitive Na+ transport. In the absence of Cl-, the response to amiloride was significantly smaller, which suggests that Cl- depletion also has an inhibitory effect on electrogenic, amiloride-sensitive Na+ absorption.
对未受刺激的马气管黏膜电解质转运的基本组成部分进行了表征。将组织安装在尤斯灌流室后，电流和组织电阻在达到稳定值之前逐渐增加约60分钟。此后，在开路条件下，组织电阻为250±14Ω·cm²，产生-34±1.7（SE）mV的跨上皮电位差（以浆膜侧为参考）和-149±10.2μA/cm²的等效短路电流（Ieqsc）。尽管10⁻⁵M氨氯吡咪使电流降低了约65%，但用胆碱替代黏膜Na⁺使电流降低得更多（约80%），这表明部分Na⁺依赖性电流对氨氯吡咪不敏感。在浆膜侧施加10⁻⁴M布美他尼后电流未降低，布美他尼预期会抑制Na⁺-K⁺-2Cl⁻介导的Cl⁻分泌，尽管用葡萄糖酸盐双侧替代Cl⁻使Ieqsc降低了约30μA/cm²。持续的短路条件导致短路电流可逆下降，该下降被氨氯吡咪抑制但不被Cl⁻耗竭抑制，这表明持续短路会导致对氨氯吡咪敏感的Na⁺转运被显著低估。在无Cl⁻的情况下，对氨氯吡咪的反应明显较小，这表明Cl⁻耗竭对电生性、氨氯吡咪敏感的Na⁺吸收也有抑制作用。
