Arginine vasopressin responses to hypoxia and hypercapnia in late-gestation fetal sheep. Am J Physiol 1991 Jun;260(6 Pt 2):R1077-81
Date
06/01/1991Pubmed ID
2058735DOI
10.1152/ajpregu.1991.260.6.R1077Scopus ID
2-s2.0-0025776216 (requires institutional sign-in at Scopus site) 63 CitationsAbstract
The purpose of this study was to determine the interaction of hypoxia and hypercapnia in the control of arginine vasopressin (AVP) secretion in fetal sheep and to determine the role of the peripheral arterial chemoreceptors in that response. We measured the plasma AVP response to hypercapnia and/or hypoxia in catheterized intact or sinoaortic-denervated fetal sheep between 123 and 144 days of gestation. Ewes were exposed to the following inspired gases: two successive 30-min periods of normocapnic normoxia, 30 min of normocapnic normoxia followed by 30 min of normocapnic hypoxia, two successive 30-min periods of hypercapnic normoxia, or 30 min of hypercapnic normoxia followed by 30 min of hypercapnic hypoxia (i.e., asphyxia). Hypercapnia per se had no significant effect on fetal plasma AVP. Normocapnic hypoxia per se resulted in a significant increase in fetal plasma AVP. Although hypercapnia resulted in a significant acidemia, the decrease in arterial pH was more marked under hypoxic conditions. Hypercapnia/acidemia augmented the AVP response to hypoxia. Fetal sinoaortic denervation did not significantly attenuate any of the AVP responses. We conclude that hypercapnia augments the fetal AVP response to hypoxia and that the AVP response to neither normocapnic nor hypercapnic hypoxia is dependent on afferent information carried in the carotid sinus or aortic nerves.
Author List
Raff H, Kane CW, Wood CEAuthor
Hershel Raff PhD Professor in the Academic Affairs department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsArginine Vasopressin
Blood Gas Analysis
Chemoreceptor Cells
Female
Hydrogen-Ion Concentration
Hypercapnia
Hypoxia
Pregnancy
Pregnancy, Animal
Sheep
