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This Article Full Text Full Text (PDF) All Versions of this Article: 90/2/189    most recent expphysiol.2004.028720v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Best, J. A. Articles by Quinton, P. M Search for Related Content PubMed PubMed Citation Articles by Best, J. A. Articles by Quinton, P. M Related Collections GI & Epithelial

¹ Department of Pediatrics, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0831, USA ² Division of Biomedical Sciences, University of California Riverside, Riverside, CA 92521-0121

Computerized assays on cultured cells ex vivo have been used to screen thousands of compounds for their effectiveness in correcting the basic physiological defect in cystic fibrosis (CF). While a number of these compounds appear promising, their effectiveness will almost certainly need to be demonstrated in animals before therapeutic tests in humans will be possible. We show herein that the function of salivary secretion in the mouse model for CF could be used as a simple, easy and rapid in vivo assay for drug effects. We demonstrate that salivary secretory capacity stimulated with a ß-adrenergic agonist closely reflects the genotype of origin. Specifically, the mean maximal secretory rate of saliva in normal wild type (+/+) mice was about 1.5 times higher than that of the mean rate in heterozygote (+/–) mice and more than 50 times greater than in CF (–/–) mice. Total saliva secreted per stimulated period obeyed a similar phenotype–genotype segregation. The data indicate that salivary secretory rates in CF mice could be used to assay potential drugs for their effectiveness in correcting the secretory defect in cystic fibrosis.

(Received 21 July 2004; accepted after revision 26 October 2004; first published online 30 November 2004)
Corresponding author P. M. Quinton: University of California, San Diego, Department of Pediatrics, 9500 Gilman Drive, La Jolla, CA 92093-0831, USA. Email: pquinton{at}ucsd.edu

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