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Am J Physiol Lung Cell Mol Physiol (May 5, 2006). doi:10.1152/ajplung.00426.2005
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Submitted on October 4, 2005
Accepted on April 6, 2006

Dopamine Activates Amiloride-Sensitive Sodium Channels in Alveolar Type 1 Cells in a Lung Slice Preparation

My N. Helms1, Julie Self2, Hui Fang Bao3, Lauren C. Job2, Lucky Jain4, and Douglas C. Eaton4*

1 Department of Physiology and The Center For Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia, United States
2 Department of Physiology and The Center for Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia, United States
3 Department of Physiology and the Center for Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia, United States
4 Department of Physiology, Pediatrics and The Center for Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia, United States

* To whom correspondence should be addressed. E-mail: deaton{at}emory.edu.

Active Na reabsorption by alveolar epithelial cells generates the driving force used to clear fluids from the air space. Using single channel methods, we examined epithelial sodium channel (ENaC) activity of ATI cells from live 250-300µm sections of lung tissue, circumventing concerns of whether protracted cell isolation procedures will compromise the innate transport properties of native lung cells. We used fluorescein-labeled erythrina crystagalli lectin to positively identify ATI cells for single channel patch clamp analysis. We demonstrate for the first time single channel recordings of highly selective and non-selective, amiloride-sensitive ENaC channels (HSC and NSC) from ATI cells in situ with mean conductances of 8.2|±2.5 pS and 22±3.2 pS, respectively. Additionally, 25nM amiloride in the patch electrode blocked Na channel activity in ATI cells. Immunohistochemical studies demonstrated the presence of dopamine D1 and D2 receptors on the surface of ATI cells, and single channel recordings show that 10µM dopamine increased Na channel activity (NPo) from 0.31±0.19 to 0.60±0.21 (p<0.001). The D1 receptor antagonist, SCH23390 (10µM), blocked the stimulatory effect of dopamine on ATI lung cells, but the D2 receptor antagonist, sulpiride, did not.




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