The role of endothelins in the regulation of pituitary function

Lange, Manfred; Pagotto, Uberto; Renner, Ulrich; Arzberger, Thomas; Oeckler, R.; Stalla, GK

doi:10.1055/s-2002-29086

Cited by 11 publications

(7 citation statements)

References 93 publications

(145 reference statements)

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“…The neuromodulatory effects of ET in the regulation of hypothalamic-pituitary function (20), the finding of ET receptors in the hypothalamus and pituitary and its CRH-like action are a good reason to suspect the pathogenetic role of ET in Cushing's disease.…”

Section: Discussionmentioning

confidence: 99%

Elevated plasma endothelin as an additional cardiovascular risk factor in patients with Cushing's syndrome

Кirilov¹,

Tomova²,

Dakovska³

et al. 2003

European Journal of Endocrinology

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Background: Recently the pathophysiological role of endothelin (ET) has been presumed in a number of adrenal disorders such as primary hyperaldosteronism, pheochromocytoma and adrenocortical insufficiency. Aim: The aim of the present study was to evaluate circulating ET-1 levels in patients with endogenous Cushing's syndrome. Methods and results: Plasma ET-1 levels were determined by highly sensitive RIA. Thirteen untreated subjects with Cushing's syndrome were studied: eight women and five men of mean age 44.2^9.5 years (S.D.). In ten of them, Cushing's disease had been diagnosed and three had adrenal adenomas. ET-1 was 3-fold higher in the patient group than in age-matched healthy controls (n ¼ 13): 1.59^0.78 vs 0.46^0.20 pmol/l respectively, P , 0.001. In adrenal adenoma patients, ET-1 was not significantly higher than in the Cushing's disease subjects (1.84^0.67 vs 1.51^0.83 pmol/l respectively, P . 0.05). In three patients who died of severe cardiovascular complications, plasma ET-1 was significantly higher than in the remaining patients (2.34^0.35 pmol/l, P , 0.05). A positive correlation was found between the total cholesterol (6.94^1.75 mmol/l) and ET-1 levels in the patients with Cushing's syndrome: r ¼ þ0.73, P , 0.02. No correlation was observed, however, between the levels of ET-1 and blood pressure (183^37/106^18 mmHg), plasma cortisol levels (455.2^74.5 nmol/l) or urinary cortisol excretion (1463^726 nmol/24 h). The successful treatment and correction of hypercortisolism in seven patients led to insignificant reduction in plasma ET from 1.34^0.69 to 0.73^0.53 pmol/l, P . 0.05. Conclusion: Our results clearly demonstrate that the ET system is activated in Cushing's syndrome. Elevated plasma ET-1 levels probably play a role in the pathogenesis of accelerated and early atherosclerosis development in this disorder.

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Section: Discussionmentioning

confidence: 99%

Elevated plasma endothelin as an additional cardiovascular risk factor in patients with Cushing's syndrome

Кirilov¹,

Tomova²,

Dakovska³

et al. 2003

European Journal of Endocrinology

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“…G protein-coupled ET receptors (29) are also present in pituitary cells and participate in the control of secretion (30). Several reports suggest that the ET-A subtype of these receptors is expressed in anterior pituitary cells (24,(31)(32)(33), whereas the ET-B receptor subtype may be expressed in the intermediate lobe of the gland (34).…”

Section: Et Inhibits Extracellular Camentioning

confidence: 99%

Endothelin-induced, Long Lasting, and Ca2+ Influx-independent Blockade of Intrinsic Secretion in Pituitary Cells by Gz Subunits

Andrić¹,

Živadinović

González-Iglesias

et al. 2005

Journal of Biological Chemistry

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influx. This action occurred through the G z signaling pathway; the adenylyl cyclase-signaling cascade could mediate sustained inhibition of secretion, whereas rapid inhibition also occurred at elevated cAMP levels regardless of the status of phospholipase C, tyrosine kinases, and protein kinase C. In a nanomolar concentration range, endothelin also inhibited voltagegated Ca 2؉ influx through the G i/o signaling pathway. Thus, the coupling of seven-transmembrane domain endothelin receptors to G z proteins provided a pathway that effectively blocked hormone secretion distal to Ca 2؉ entry, whereas the cross-coupling to G i/o proteins reinforced such inhibition by simultaneously reducing the pacemaking activity.

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“…Implication here means that synthetic machinery for ET peptides, ET peptides themselves, and ET receptors have been localized to tissues in these systems, as well as demonstration that ET-1 causes a physiological function within that system. An incomplete list includes the cardiovascular (11,12,16,98), renal (35,58,87), central nervous (103), gastrointestinal (45), pituitary (61), adrenal (24,43,95,96), nasal (83), peripheral nervous (20,33,82), immune (76), hepatic (70), genitourinary (15), and endocrine systems (75).…”

mentioning

confidence: 99%

Endothelin receptors: what's new and what do we need to know?

Watts

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Receptors are at the heart of how a molecule transmits a signal to a cell. Two receptor classes for endothelin (ET) are recognized, the ET(A) and ET(B) receptors. Intriguing questions have arisen in the field of ET receptor pharmacology, physiology, and function. For example, a host of pharmacological studies support the interaction of the ET(A) and ET(B) receptor in tissues (veins, arteries, bronchus, arterioles, esophagus), but yet few have been able to demonstrate direct ET(A)/ET(B) receptor interaction. Have we modeled this interaction wrong? Do we have a truly selective ET(A) receptor agonist such that we could selectively stimulate this important receptor? What can we learn from the recent phylogenic studies of the ET receptor family? Have we adequately addressed the number of biological molecules with which ET can interact to exert a biological effect? Recent mass spectrometry studies in our laboratory suggest that ET-1 interacts with other hereto unrecognized proteins. Biased ligands (ligands at the same receptor that elicit distinct signaling responses) have been discovered for other receptors. Do these exist for ET receptors and can we take advantage of this possibility in drug design? These and other questions will be posed in this minireview on topics on ET receptors.

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The role of endothelins in the regulation of pituitary function

Cited by 11 publications

References 93 publications

Elevated plasma endothelin as an additional cardiovascular risk factor in patients with Cushing's syndrome

Elevated plasma endothelin as an additional cardiovascular risk factor in patients with Cushing's syndrome

Endothelin-induced, Long Lasting, and Ca2+ Influx-independent Blockade of Intrinsic Secretion in Pituitary Cells by Gz Subunits

Endothelin receptors: what's new and what do we need to know?

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