Evidence for a Role of Vasopressin in the Control of Aldosterone Secretion in Primary Aldosteronism:<i>in Vitro</i>and<i>in Vivo</i>Studies

Perraudin, Véronique; Delarue, Catherine; Lefebvre, Henri; Rego, Jean-Luc do; Vaudry, Hubert; Kuhn, Jean-Marc

doi:10.1210/jc.2005-1453

Cited by 48 publications

(32 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We used C t Z39 as the cutoff for considering the real-time results as positive. Standard curves with increasing concentrations of cDNA (5,10,20,40, and 80 ng) obtained from a pool of normal adrenals were obtained for all genes to verify the reaction efficiency: this was judged to be good when the slope came between 3.2 and 3.6. Water was used as a nontemplate control, while nonreverse-transcribed samples were run in parallel with the reverse-transcribed samples to rule out false-positive reactions.…”

Section: Real-time Rt-pcr Quantificationmentioning

confidence: 99%

“…Only a few studies have examined the possible role of the aberrant expression of G-protein-coupled receptors (GPCRs) in the adrenocortical tissue of patients with aldosterone-producing adenomas (APA) (3)(4)(5). Although an overexpression of LH and/or GNRH receptors (LHR and GNRHR) has been demonstrated in some APA (6,7), less is known about the aldosterone response to in vivo GNRH or LH in these patients (8).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

A case of primary aldosteronism in pregnancy: do LH and GNRH receptors have a potential role in regulating aldosterone secretion?

Albiger¹,

Sartorato²,

Mariniello³

et al. 2011

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: The mechanisms inducing steroidogenesis in primary aldosteronism (PA) remain poorly defined. It was recently demonstrated that some G-protein-coupled receptors are abnormally expressed in aldosterone-producing adenomas (APA). We evaluated the potential role of LH and GNRH receptors (LHR (or LHCGR) and GNRHR) in regulating aldosterone secretion in a patient with APA arising during pregnancy (index case) and in a subset of other patients with PA. Patients and methods: GNRH test was performed in the index case, 11 other PA, and 5 controls. GNRHR and LHR expressions were examined in 23 APA and 6 normal tissues. Results: Aldosterone response increased significantly (114%) in the index case after GNRH test was performed preoperatively, while it was blunted after adrenalectomy. Aldosterone also increased after human chorionic gonadotropin and triptorelin stimulation. A partial aldosterone response to GNRH was observed in other 7/11 PA, while a significant response was observed in two patients. Controls did not respond to GNRH test. GNRHR was overexpressed and LHR expression was moderate in the APA tissue from the index case. Moreover, LHR was found in normal adrenals and overexpressed in 6/22 APA. GNRHR was overexpressed in 6/22 APA, 2 of them with a 95-and 109-fold higher expression than normal. A correlation between the clinical and molecular findings was observed in five out of seven patients. Conclusion: We describe a case of PA diagnosed during pregnancy, which appeared to correlate with aberrant LHR and GNRHR expression. Our findings suggest that a subset of patients with PA has aberrant LHR and GNRHR expression, which could modulate aldosterone secretion.

show abstract

Section: Real-time Rt-pcr Quantificationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A case of primary aldosteronism in pregnancy: do LH and GNRH receptors have a potential role in regulating aldosterone secretion?

Albiger¹,

Sartorato²,

Mariniello³

et al. 2011

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Among the 19 cases of corticomedullary mixed tumors reported in the literature, seven patients presented catecholamine overproduction that was associated with hypercortisolism in three cases (57,59,60). In very much the same way, our group has described the occurrence of clusters of chromogranin A-positive chromaffin cells disseminated in adrenocortical adenoma responsible for hyperaldosteronism (61) or subclinical Cushing's syndrome (62).…”

Section: Sources Of Paracrine Regulatory Factors In Adrenocortical Nementioning

confidence: 79%

“…The increased sensitivity of adrenocortical cells to AVP has been ascribed to overexpression of the eutopic V1a receptor subtype (120,125,126,127) and/or expression of ectopic V1b and V2 receptors (127,128,129). Similarly, mRNAs encoding the V1a and V2 receptors have been detected at variable levels in aldosteroneproducing adenomas (61,130,131). In vitro pharmacological experiments have revealed that the aldosterone response to AVP is mediated by activation of V1a receptors (61).…”

Section: Factorsmentioning

confidence: 99%

“…Similarly, mRNAs encoding the V1a and V2 receptors have been detected at variable levels in aldosteroneproducing adenomas (61,130,131). In vitro pharmacological experiments have revealed that the aldosterone response to AVP is mediated by activation of V1a receptors (61). Only a few clinical studies have evaluated the effect of vasopressin receptor antagonists in patients with primary adrenal steroid excess.…”

Section: Factorsmentioning

confidence: 99%

See 1 more Smart Citation

MECHANISMS IN ENDOCRINOLOGY: Autocrine/paracrine regulatory mechanisms in adrenocortical neoplasms responsible for primary adrenal hypercorticism

Lefebvre

Prévost

Louiset

2013

European Journal of Endocrinology

View full text Add to dashboard Cite

A wide variety of autocrine/paracrine bioactive signals are able to modulate corticosteroid secretion in the human adrenal gland. These regulatory factors, released in the vicinity of adrenocortical cells by diverse cell types comprising chromaffin cells, nerve terminals, cells of the immune system, endothelial cells, and adipocytes, include neuropeptides, biogenic amines, and cytokines. A growing body of evidence now suggests that paracrine mechanisms may also play an important role in the physiopathology of adrenocortical hyperplasias and tumors responsible for primary adrenal steroid excess. These intra-adrenal regulatory systems, although globally involving the same actors as those observed in the normal gland, display alterations at different levels, which reinforce the capacity of paracrine factors to stimulate the activity of adrenocortical cells. The main modifications in the adrenal local control systems reported by now include hyperplasia of cells producing the paracrine factors and abnormal expression of the latter and their receptors. Because steroid-secreting adrenal neoplasms are independent of the classical endocrine regulatory factors angiotensin II and ACTH, which are respectively suppressed by hyperaldosteronism and hypercortisolism, these lesions have long been considered as autonomous tissues. However, the presence of stimulatory substances within the neoplastic tissues suggests that steroid hypersecretion is driven by autocrine/paracrine loops that should be regarded as promising targets for pharmacological treatments of primary adrenal disorders. This new potential therapeutic approach may constitute an alternative to surgical removal of the lesions that is classically recommended in order to cure steroid excess.European Journal of Endocrinology 169 R115-R138

show abstract

Steroidogenesis—Adrenal Cell Signal Transduction

Gallo‐Payet

Battista

2014

Comprehensive Physiology

View full text Add to dashboard Cite

The purpose of this article is to review fundamentals in adrenal gland histophysiology. Key findings regarding the important signaling pathways involved in the regulation of steroidogenesis and adrenal growth are summarized. We illustrate how adrenal gland morphology and function are deeply interconnected in which novel signaling pathways (Wnt, Sonic hedgehog, Notch, β-catenin) or ionic channels are required for their integrity. Emphasis is given to exploring the mechanisms and challenges underlying the regulation of proliferation, growth, and functionality. Also addressed is the fact that while it is now well-accepted that steroidogenesis results from an enzymatic shuttle between mitochondria and endoplasmic reticulum, key questions still remain on the various aspects related to cellular uptake and delivery of free cholesterol. The significant progress achieved over the past decade regarding the precise molecular mechanisms by which the two main regulators of adrenal cortex, adrenocorticotropin hormone (ACTH) and angiotensin II act on their receptors is reviewed, including structure-activity relationships and their potential applications. Particular attention has been given to crucial second messengers and how various kinases, phosphatases, and cytoskeleton-associated proteins interact to ensure homeostasis and/or meet physiological demands. References to animal studies are also made in an attempt to unravel associated clinical conditions. Many of the aspects addressed in this article still represent a challenge for future studies, their outcome aimed at providing evidence that the adrenal gland, through its steroid hormones, occupies a central position in many situations where homeostasis is disrupted, thus highlighting the relevance of exploring and understanding how this key organ is regulated. © 2014 American Physiological Society. Compr Physiol 4:889-964, 2014.

show abstract

Evidence for a Role of Vasopressin in the Control of Aldosterone Secretion in Primary Aldosteronism:in Vitroandin VivoStudies

Abstract: The present study indicates that functional V(1a) receptors are present in APA and suggests that AVP may exert an autocrine/paracrine control of aldosterone secretion in APA tissues.

Cited by 48 publications

References 39 publications

A case of primary aldosteronism in pregnancy: do LH and GNRH receptors have a potential role in regulating aldosterone secretion?

A case of primary aldosteronism in pregnancy: do LH and GNRH receptors have a potential role in regulating aldosterone secretion?

MECHANISMS IN ENDOCRINOLOGY: Autocrine/paracrine regulatory mechanisms in adrenocortical neoplasms responsible for primary adrenal hypercorticism

Steroidogenesis—Adrenal Cell Signal Transduction

Contact Info

Product

Resources

About