Upregulation of V1a vasopressin receptors by glucocorticoids

Colson, P; Ibarondo, J.; Devilliers, Ginette; Balestre, Marie-Noëlle; Duvoid, A.; Guillon, Gilles

doi:10.1152/ajpendo.1992.263.6.e1054

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…In vitro studies have shown that incubation of vascular smooth muscle cells with dexamethasone enhances the increase in IP formation by these hormones (42,43), though others using a similar experimental system have reported uncoupling of the Ang II receptor by glucocorticoids (44). In contrast to the pituitary V1b-R, vascular smooth muscle Ang and V1a receptors increase after in vitro incubation with glucocorticoids (45,46), which would also contribute to the sensitizing action of glucocorticoids.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids Increase Vasopressin V1b Receptor Coupling to Phospholipase C

Rabadan‐Diehl¹,

Aguilera²

1998

Endocrinology

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Vasopressin (VP) stimulates pituitary ACTH secretion after binding to V1b VP receptors (V1b-R) coupled to phospholipase C (PLC). This effect of VP on ACTH secretion, unlike that of CRH, is resistant to glucocorticoid feedback. To determine whether changes in V1b-R expression or signaling mediate the refractoriness to glucocorticoids, the effects of glucocorticoids on pituitary VP binding, V1b-R messenger RNA (mRNA) and VP-stimulated inositol phosphate (IP) formation were studied in vivo and in vitro in the rat. Dexamethasone injection for 7 days decreased VP binding but increased V1b-R mRNA, indicating that mRNA levels do not reflect receptor number. In spite of the binding loss, VP-stimulated IP formation was enhanced in dexamethasone-treated rats, suggesting that glucocorticoids increase the coupling efficiency of the V1b receptor to phospholipase C. Pretreatment of pituitary cells in vitro with dexamethasone or corticosterone, also potentiated IP formation by low and high doses of VP, indicating that glucocorticoids act directly in the pituitary and not through changes in hypothalamic factors. The effect is mediated by glucocorticoid receptors because it was blocked by glucocorticoid but not mineralocorticoid antagonists. Dexamethasone potentiated the stimulation of IP by other PLC-dependent ligands (GnRH, TRH) but not that by the calcium ionophore, ionomycin, suggesting a site of action between the receptor and PLC. After treatment with dexamethasone, in vivo or in vitro, Western blot analysis revealed marked increases in the GTP binding protein, Galpha(q), which may account for the potentiating effect of glucocorticoid on ligand-stimulated IP. The data demonstrate that glucocorticoids increase coupling of the V1b-R with PLC thereby providing a mechanism by which VP facilitates corticotroph responsiveness in spite of elevated levels of plasma glucocorticoids during stress.

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Section: Discussionmentioning

confidence: 99%

Glucocorticoids Increase Vasopressin V1b Receptor Coupling to Phospholipase C

Rabadan‐Diehl¹,

Aguilera²

1998

Endocrinology

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“…In other vertebrates, neural AVT protein and pro-AVT mRNA levels are both regulated by gonadal steroids [21,43], and gonadal steroids and glucocorticoids have been shown to regulate AVT/AVP receptor density in select brain regions of mammals (e.g., [7,29,68,71]). AVT receptor mRNAs in the hindbrain have been shown to vary seasonally in teleosts [62], but no study has yet examined whether v1a2 gene transcription in the teleost brain is regulated by steroid hormones.…”

Section: Variation In V1a-type Receptor Mrna Abundance Among Sexual Pmentioning

confidence: 99%

Variation in gene transcript profiles of two V1a-type arginine vasotocin receptors among sexual phases of bluehead wrasse (Thalassoma bifasciatum)

Lema

Slane

Salvesen

et al. 2012

General and Comparative Endocrinology

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“…The elevation of mRNA levels precedes the rise in binding activity, suggesting a transcriptional effect. Furthermore, it has been reported that GC amplify the vasopressin-induced transduction signal (increased IP accumulation in the presence of dexamethasone) (312,313). At the protein level, GC have been shown to produce an early decrease in binding site density, followed later by an increase, which becomes more prevalent with time.…”

Section: A Tissue-specific Expression and Regulation Of Membrane Hormentioning

confidence: 99%

Ectopic and Abnormal Hormone Receptors in Adrenal Cushing’s Syndrome*

et al. 2001

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The mechanism by which cortisol is produced in adrenal Cushing's syndrome, when ACTH is suppressed, was previously unknown and was referred to as being "autonomous." More recently, several investigators have shown that some cortisol and other steroid-producing adrenal tumors or hyperplasias are under the control of ectopic (or aberrant, illicit, inappropriate) membrane hormone receptors. These include ectopic receptors for gastric inhibitory polypeptide (GIP), beta-adrenergic agonists, or LH/hCG; a similar outcome can result from altered activity of eutopic receptors, such as those for vasopressin (V1-AVPR), serotonin (5-HT4), or possibly leptin. The presence of aberrant receptors places adrenal cells under stimulation by a trophic factor not negatively regulated by glucocorticoids, leading to increased steroidogenesis and possibly to the proliferative phenotype. The molecular mechanisms responsible for the abnormal expression and function of membrane hormone receptors are still largely unknown. Identification of the presence of these illicit receptors can eventually lead to new pharmacological therapies as alternatives to adrenalectomy, now demonstrated by the long-term control of ectopic P-AR- and LH/hCGR-dependent Cushing's syndrome by propanolol and leuprolide acetate. Further studies will potentially identify a larger diversity of hormone receptors capable of coupling to G proteins, adenylyl cyclase, and steroidogenesis in functional adrenal tumors and probably in other endocrine and nonendocrine tumors.

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Upregulation of V1a vasopressin receptors by glucocorticoids

Cited by 13 publications

References 32 publications

Glucocorticoids Increase Vasopressin V1b Receptor Coupling to Phospholipase C

Glucocorticoids Increase Vasopressin V1b Receptor Coupling to Phospholipase C

Variation in gene transcript profiles of two V1a-type arginine vasotocin receptors among sexual phases of bluehead wrasse (Thalassoma bifasciatum)

Ectopic and Abnormal Hormone Receptors in Adrenal Cushing’s Syndrome*

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