Adrenocortical function in a new world primate, the marmoset monkey, Callithrix jacchus

Citation
Bj. Whitehouse et Dre. Abayasekara, Adrenocortical function in a new world primate, the marmoset monkey, Callithrix jacchus, GEN C ENDOC, 120(1), 2000, pp. 2-7
Citations number
29
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
GENERAL AND COMPARATIVE ENDOCRINOLOGY
ISSN journal
00166480 → ACNP
Volume
120
Issue
1
Year of publication
2000
Pages
2 - 7
Database
ISI
SICI code
0016-6480(200010)120:1<2:AFIANW>2.0.ZU;2-D
Abstract
The function of the adrenal cortex of the marmoset monkey Callithrix jacchu s has been investigated. In common with other New World primates, these ani mals seem to be glucocorticoid resistant. Blood and adrenal glands were obt ained from male and female animals under terminal pentobarbitone anesthesia . Dispersed adrenal cell preparations were obtained by treatment with colla genase and incubated with ACTH(1-24), (0.1-1000 nM) angiotensin II (0.1-100 0 nM), dibutyryl cyclic AMP (dbcAMP; 30-1000 muM), and forskolin (FSK; 1-30 muM). Plasma cortisol levels (2113 +/- 449 ng/ml male; 3858 +/- 429 ng/ml female) were found to be 10- to 20-fold higher than those quoted for Old Wo rld primates and man. The cell preparations showed no significant response to any dose of ACTH tested (0.1-1000 nM), although addition of exogenous pr ecursor (22R-hydroxycholesterol, 2.5 muM) resulted:in an increased yield of cortisol and aldosterone. Cyclic AMP production was increased in response to forskolin (1-30 muM) but not ACTH(1-24) (1-1000 nM). In addition, dose-r elated responses to angiotensin II (maximal stimulation of 316 +/- 49% basa l aldosterone at 100 nM angiotensin II), dbcAMP (maximal stimulation of 449 +/- 24% basal cortisol at 300 muM dbcAMP), and forskolin (maximal stimulat ion of 394 +/- 31% basal cortisol at 10 muM FSK) were obtained. The lack of a response in vitro to ACTH in C. jacchus cannot, therefore, be attributed either to general failure of the cells or to defects in postreceptor signa ling mechanisms. The results suggest that there is a reduction in adrenal A CTH receptor number or affinity, with a high basal production rate in vivo maintaining the elevated plasma cortisol levels. (C) 2000 Academic Press.