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Vasopressin Receptor Expression in the Placenta

Howard Florey Institute of Experimental Physiology and Medicine,² The University of Melbourne, 3010 Victoria, Australia Department of Medicine,³ The University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg, 3084 Victoria, Australia Departments of Physiology⁴ Anatomy and Cell Biology,⁵ Monash University, Clayton, 3800 Victoria, Australia

The arginine vasopressin (AVP) type 1a receptor (V1a) is well known to mediate vasoconstriction. In pregnancy, blood flow in the placenta is crucial for sustaining normal growth and development of the fetus. This is the first AVP receptor study in the placenta and fetal membranes. The aim was to compare, quantitatively, the level of V1a gene expression with that of a known marker for vascularization, aquaporin 1 (AQP1). V1a and AQP1 gene expression did not correlate; placental V1a mRNA levels were significantly upregulated at 45 and 66 ± 1 compared with 27, 100 ± 4, and 140 days (term 150 days). V1a mRNA levels were much lower in fetal membranes in which no significant difference across gestation was observed. In situ hybridization histochemistry localized V1a gene expression in the maternal component of the placenta similar to the receptor-binding studies using ¹²⁵I-labeled [d(CH₂)₅, sarcosine⁷] vasopressin. No AVP gene expression was observed in the placenta and fetal membranes, which eliminates local AVP production. This increase in V1a expression at 45 and 66 ± 1 days of gestation correlates with the period of maximal placental growth in the sheep and suggests that AVP and V1a receptors may play a hitherto unrecognized role in placental growth, differentiation, and/or function, particularly in the deleterious effects of heat stress, early in pregnancy, on fetal growth.

¹ Correspondence: Marelyn Wintour, Department of Physiology, Monash University, Clayton, 3800 Victoria, Australia. FAX: 61 3 9905 2547; mwc{at}med.monash.edu.au

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