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J. Biol. Chem., Vol. 281, Issue 38, 27964-27972, September 22, 2006

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Molecular Identification and Physiological Roles of Parotid Acinar Cell Maxi-K Channels^*

Victor Romanenko¹, Tetsuji Nakamoto¹, Alaka Srivastava, James E. Melvin, and Ted Begenisich²

From the Department of Pharmacology and Physiology and the Center for Oral Biology, Aab Institute of Biomedical Sciences, University of Rochester Medical Center, Rochester, New York 14642

The physiological success of fluid-secreting tissues relies on a regulated interplay between Ca²⁺-activated Cl^– and K⁺ channels. Parotid acinar cells express two types of Ca²⁺-activated K⁺ channels: intermediate conductance IK1 channels and maxi-K channels. The IK1 channel is encoded by the K_Ca3.1 gene, and the K_Ca1.1 gene is a likely candidate for the maxi-K channel. To confirm the genetic identity of the maxi-K channel and to probe its specific roles, we studied parotid glands in mice with the K_Ca1.1 gene ablated. Parotid acinar cells from these animals lacked maxi-K channels, confirming their genetic identity. The stimulated parotid gland fluid secretion rate was normal, but the sodium and potassium content of the secreted fluid was altered. In addition, we found that the regulatory volume decrease in acinar cells was substantially impaired in K_Ca1.1-null animals. We examined fluid secretion from animals with both K⁺ channel genes deleted. The secretion rate was severely reduced, and the ion content of the secreted fluid was significantly changed. We measured the membrane potentials of acinar cells from wild-type mice and from animals with either or both K⁺ channel genes ablated. They revealed that the observed functional effects on fluid secretion reflected alterations in cell membrane voltage. Our findings show that the maxi-K channels are critical for the regulatory volume decrease in these cells and that they play an important role in the sodium uptake and potassium secretion process in the ducts of these fluid-secreting salivary glands.

Received for publication, April 21, 2006 , and in revised form, June 29, 2006.

^* This work was supported by National Institutes of Health Grants DE13539 (to J. E. M.) and DE016960 (to T. B.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Both authors contributed equally to this work.

² To whom correspondence should be addressed: Dept. of Pharmacology and Physiology, University of Rochester Medical Center, P. O. Box 711, Rochester, NY 14642. Tel.: 585-275-3456; Fax: 585-273-2652; E-mail: Ted_Begenisich{at}URMC.rochester.edu.

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