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This version published online on October 2, 2003
Endocrinology, doi:10.1210/en.2003-1130
A more recent version of this article appeared on January 1, 2004
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Submitted on August 28, 2003
Accepted on September 22, 2003

Basal and ACTH-stimulated corticosterone in the neonatal rat exposed to hypoxia from birth: modulation by chemical sympathectomy a

Hershel Raff1*, Julie J. Lee1, Eric P. Widmaier1, Martin K. Oaks1, and William C. Engeland1

1 Endocrine and Transplant Research Laboratories, St. Luke's Medical Center, Milwaukee, WI 53215; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226; Department of Biology, Boston University, Boston, MA 02215; Depts of Surgery and Neuroscience, University of Minnesota, Minneapolis, MN 55455

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

We previously demonstrated that 7-day old rat pups exposed to hypoxia from birth exhibit ACTH-independent increases in corticosterone associated with an increase in StAR and PBR proteins. The purpose of the present study was to determine if this increase in corticosterone could be attenuated by chemical sympathectomy induced with guanethidine treatment. Rat pups were exposed to normoxia or hypoxia from birth and treated with vehicle or guanethidine and studied at 7 days of age. Hypoxia per se resulted in an increase in plasma corticosterone without a change in plasma ACTH. Guanethidine treatment attenuated the increase in basal corticosterone in hypoxic pups, but did not attenuate ACTH-stimulated corticosterone production. This effect was specific as basal and ACTH-stimulated aldosterone was not affected. Guanethidine also attenuated the increase in StAR protein induced by hypoxia. Neither the effect of hypoxia nor guanethidine could be explained by changes in the levels of adrenal tyrosine hydroxylase, StAR, or P450scc mRNA, adrenal tyrosine hydroxylase immunohistochemistry, or adrenal catecholamine content. We conclude that chemical sympathectomy normalizes basal corticosterone levels but has no effect on ACTH-stimulated corticosterone levels in 7 day-old rats exposed to hypoxia from birth. The mechanism of the effect of guanethidine to normalize hypoxia-stimulated basal corticosterone remains to be identified, although StAR protein may be an important mediator. This ACTH-independent increase in corticosterone may be a mechanism by which the neonate can increase circulating glucocorticoids necessary for survival, while bypassing the hyporesponsiveness of the neonatal hypothalamic-pituitary-adrenal axis.
Key words: adrenal cortex • newborn • adrenocorticotropin • anoxia • tyrosine hydroxylase • steroidogenic acute regulatory (StAR) protein




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