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- Title
Eutopic overexpression of vasopressin v1a receptor in adrenocorticotropin-independent macronodular adrenal hyperplasia.
- Authors
TOMOATSU MUNE; HIROSHI MURASE; NORIYOSHI YAMAKITA; TETSUYA FUKUDA; MASANORI MURAYAMA; ATSUSHI MIURA; TETSUYA SUWA; JUNKO HANAFUSA; HISASHI DAIDO; HIROYUKI MORITA; KEIGO YASUDA
- Abstract
Arginine vasopressin (AVP) stimulates cortisol secretion through its vascular type V1a receptor in the adrenal glands, in addition to stimulating ACTH secretion through pituitary V3 receptor. Because hyper-response of plasma cortisol to vasopressin is documented in some patients with Cushing's syndrome due to adrenal adenoma (CS) or ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), we analyzed the expression of V1a, V2, V3 receptor and AVP mRNA in human adrenal tissues by quantitative competitive RT-PCR or real-time PCRs. V(1a) receptor mRNA levels (ratio against glyceraldehyde 3-phosphate dehydrogenase) were 0.378 +/- 0.143 (mean +/- SE) in preclinical CS (n = 5) and 0.630 +/- 0.072 in AIMAH (n = 4), which were significantly higher than those (0.046 +/- 0.012; n = 9) in control adrenals, whereas those in overt CS (0.143 +/- 0.048; n = 10) or aldosterone-producing adenomas (0.069 +/- 0.018; n = 12) were similar to control adrenals. Although ectopic expression of V2 or V3 receptor was detected in half of AIMAH cases, the absolute levels were low. Furthermore, V1a receptor mRNA levels in the adjacent adrenal glands (0.190 +/- 0.039, n = 9) of aldosterone-producing adenomas were higher than those in control adrenals and in the corresponding tumor portions (0.079 +/- 0.024). In contrast, there were no significant differences in AVP mRNA levels among these groups. These results suggest that eutopic V1a receptor overexpression is involved in the etiology of AIMAH and a subset of adrenal adenomas causing overt or preclinical Cushing's syndrome. Our results imply a possible association of V1a receptor expression with adrenal hyperplasia.
- Publication
Journal of Clinical Endocrinology & Metabolism, 2002, Vol 87, Issue 12, p5706
- ISSN
0021-972X
- Publication type
Article
- DOI
10.1210/jc.2002-020067