Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol 104: 803-808, 2008. First published December 20, 2007; doi:10.1152/japplphysiol.00393.2007
8750-7587/08 $8.00
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Sustained hypoxia-induced proliferation of carotid body type I cells in rats

Z.-Y. Wang,1 E. B. Olson, Jr.,3 D. E. Bjorling,1 G. S. Mitchell,2 and G. E. Bisgard2

Departments of 1Surgical Sciences, 2Comparative Biosciences and 3Population Health Sciences, University of Wisconsin-Madison, Madison, Wisconsin

Submitted 12 April 2007 ; accepted in final form 14 December 2007

Sustained hypoxia (SH) has been shown to cause profound morphological and cellular changes in carotid body (CB). However, results regarding whether SH causes CB type I cell proliferation are conflicting. By using bromodeoxyuridine, a uridine analog that is stably incorporated into cells undergoing DNA synthesis, we have found that SH causes the type I cell proliferation in the CB; the proliferation occurs mainly during the first 1–3 days of hypoxic exposure. Moreover, the new cells survive for at least 1 mo after the return to normoxia. Also, SH does not cause any cell death in CB as examined by the terminal deoxynucleotidyl transferase-mediated dUTP-X nick-end labeling assay. Taken together, our results suggest that SH stimulates CB type I cell proliferation, which may produce long-lasting changes in CB morphology and function.

bromodeoxyuridine; terminal deoxynucleotidyl transferase-mediated dUTP-X nick end-labeling assay; chemoreceptor; mitosis


Address for reprint requests and other correspondence: Z.-Yi Wang, Dept. of Surgical Sciences, School of Veterinary Medicine, Univ. of Wisconsin-Madison, 2015 Linden Dr., Madison, WI 53706 (e-mail: wangz{at}svm.vetmed.wisc.edu)






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