Evidence for glucocorticoid regulation of the rat vasopressin V1a receptor gene

Jyoti J. Watters; Michael W. Swank; Charles W. Wilkinson; Daniel M. Dorsa

doi:10.1016/0196-9781(95)02085-3

Evidence for glucocorticoid regulation of the rat vasopressin V_1a receptor gene

Jyoti J. Watters, Michael W. Swank, Charles W. Wilkinson, Daniel M. Dorsa

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

Abstract

WRK-1 cells express vasopressin V_1a receptors. Twenty-four-hour treatment of these cells with dexamethasone (DEX) resulted in an increase in [³H]AVP binding that was maximal at 12 h, and could be blocked by addition of RU 38486. The increases in [³H]AVP binding were paralleled by increases in V_1a receptor mRNA. The in vivo effects of glucocorticoids (GCs) on V_1a receptor binding in hepatic tissue were also investigated in adrenalectomized and hormone-replaced rats given either DEX or aldosterone (ALDO). DEX effectively increased V_1a receptor binding site density whereas ALDO had no effect. The DEX effects on V_1a receptor mRNA and binding strongly implicate glucocorticoids in the regulation of V_1a receptor gene expression.

Original language	English (US)
Pages (from-to)	67-73
Number of pages	7
Journal	Peptides
Volume	17
Issue number	1
DOIs	https://doi.org/10.1016/0196-9781(95)02085-3
State	Published - 1996
Externally published	Yes

Keywords

Adrenalectomy
Aldosterone
Glucocorticoid response element
Glucocorticoids
Liver
Messenger RNA
Receptor binding
Transcriptional regulation
WRK-1 cells

ASJC Scopus subject areas

Biochemistry
Physiology
Endocrinology
Cellular and Molecular Neuroscience

Access to Document

10.1016/0196-9781(95)02085-3

Cite this

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title = "Evidence for glucocorticoid regulation of the rat vasopressin V1a receptor gene",

abstract = "WRK-1 cells express vasopressin V1a receptors. Twenty-four-hour treatment of these cells with dexamethasone (DEX) resulted in an increase in [3H]AVP binding that was maximal at 12 h, and could be blocked by addition of RU 38486. The increases in [3H]AVP binding were paralleled by increases in V1a receptor mRNA. The in vivo effects of glucocorticoids (GCs) on V1a receptor binding in hepatic tissue were also investigated in adrenalectomized and hormone-replaced rats given either DEX or aldosterone (ALDO). DEX effectively increased V1a receptor binding site density whereas ALDO had no effect. The DEX effects on V1a receptor mRNA and binding strongly implicate glucocorticoids in the regulation of V1a receptor gene expression.",

keywords = "Adrenalectomy, Aldosterone, Glucocorticoid response element, Glucocorticoids, Liver, Messenger RNA, Receptor binding, Transcriptional regulation, WRK-1 cells",

author = "Watters, {Jyoti J.} and Swank, {Michael W.} and Wilkinson, {Charles W.} and Dorsa, {Daniel M.}",

note = "Funding Information: This work was supportebdy NIH Grant NS20311 (D.M.D.), the De-partmento f Veterans Affairs, and the Pharmacological Sciences Training Grant 670489 (J.J.W.). We would like to thank Dr. Stephen Lolait for supplying the vasopressin V,, receptor cDNA, Roussel Uclaf for supplying us with the RU 38486 compound, Dr. Marie Monaco for providing the WRK-1 cells, and Dr. Craig Ferris for supplying the iodinated V,, receptor antagonist. We would also like to thank Cong Xu, Jennifer Tul-lis, Monique Adams, and Tracy Bale for their laboratory assistancea nd help with the animal work.",

year = "1996",

doi = "10.1016/0196-9781(95)02085-3",

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pages = "67--73",

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AU - Watters, Jyoti J.

AU - Swank, Michael W.

AU - Wilkinson, Charles W.

AU - Dorsa, Daniel M.

N1 - Funding Information: This work was supportebdy NIH Grant NS20311 (D.M.D.), the De-partmento f Veterans Affairs, and the Pharmacological Sciences Training Grant 670489 (J.J.W.). We would like to thank Dr. Stephen Lolait for supplying the vasopressin V,, receptor cDNA, Roussel Uclaf for supplying us with the RU 38486 compound, Dr. Marie Monaco for providing the WRK-1 cells, and Dr. Craig Ferris for supplying the iodinated V,, receptor antagonist. We would also like to thank Cong Xu, Jennifer Tul-lis, Monique Adams, and Tracy Bale for their laboratory assistancea nd help with the animal work.

PY - 1996

Y1 - 1996

N2 - WRK-1 cells express vasopressin V1a receptors. Twenty-four-hour treatment of these cells with dexamethasone (DEX) resulted in an increase in [3H]AVP binding that was maximal at 12 h, and could be blocked by addition of RU 38486. The increases in [3H]AVP binding were paralleled by increases in V1a receptor mRNA. The in vivo effects of glucocorticoids (GCs) on V1a receptor binding in hepatic tissue were also investigated in adrenalectomized and hormone-replaced rats given either DEX or aldosterone (ALDO). DEX effectively increased V1a receptor binding site density whereas ALDO had no effect. The DEX effects on V1a receptor mRNA and binding strongly implicate glucocorticoids in the regulation of V1a receptor gene expression.

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