Estrogen increases renal oxytocin receptor gene expression

Nancy L. Ostrowski^*, W. Scott Young, III, and Stephen J. Loliat

Laboratory of Cell Biology¹ and ^*Office of the Director, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-4068

Endocrinology 136: 1801-1804, 1995

Estrogens have been implicated in the sodium and fluid imbalances associated with the menstrual cycle and late pregnancy. An estrogen-dependent role for renal oxytocin receptors in fluid homeostasis is suggested by our findings that estradiol benzoate treatment increases the expression of the oxytocin receptor messenger ribonucleic acid and ¹²⁵I-OTA binding to oxytocin receptors in the renal cortex and medullary collecting ducts of ovariectomized female rats. Moreover, estradiol induced high levels of oxytocin receptor expression in outer stripe proximal tubules of ovariectomized female and adrenalectomized male rats. Proximal tubule induction was inhibited in a dose-dependent manner by the anti-estrogen tamoxifen, but cortical expression of oxytocin receptors in macula densa cells was unaffected by tamoxifen. These data demonstrate cell-specific regulation of oxytocin receptor expression in macula densa and proximal tubule cells, and suggest an important role for these receptors in mediating estrogen-induced alterations in renal fluid dynamics by possibly affecting glomerular filtration and water and solute reabsorption during high estrogen states.

Estrogen-induced expression of kidney oxytocin receptors
(yellow indicates oxytocin receptor transcripts, which are
particularly abundant in the outer stripe of the outer medulla)

¹Now the Laboratory of Cellular and Molecular Regulation

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