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Articles in PresS, published online ahead of print October 3, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00427.2002
Submitted on July 17, 2002
Accepted on September 24, 2002
1 Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
2 Department of Obstetrics/Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
3 Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA; Department of Obstetrics/Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
* To whom correspondence should be addressed. E-mail: sflohr{at}wfubmc.edu.
Corticotroph responsiveness to arginine vasopressin (AVP) increases during late gestation in fetal sheep. The mechanism of this increase in AVP responsiveness is currently unknown but could be related to an increase in vasopressin type 1b (V1b) receptor expression in the pituitary during development. To determine if there are ontogenic changes in V1b receptor expression that may help explain the changes in ACTH responses to AVP, we studied pituitaries from three groups of fetal sheep (100, 120, or 140 days gestational age (dGA)). V1b receptor mRNA and protein significantly decreased by 140dGA. Peak V1b mRNA levels were detected at 100dGA, while peak V1b protein levels were detected at 120dGA. The reduction in V1b receptor expression in late gestation may be due to the naturally occurring peripartum increase in fetal plasma cortisol since cortisol infusion at 122-130dGA decreased V1b receptor mRNA. Thus, there is a marked decrease in the expression of the V1b receptor in the pituitary during fetal development leaving the role of the V1b receptor in increasing AVP responsiveness uncertain.
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