Adrenocortical Response Profiles to Corticotrophin-Releasing Hormone and Adrenocorticotrophin Challenge in the Chronically Catheterized Adult Guinea-Pig

Abstract

summaryThe guinea-pig has been used extensively to investigate adrenal steroidogenesis. However, very little is known about adrenocortical responses to corticotrophin-releasing hormone (CRH) and adrenocorticotrophin (ACTH) in this species, in vivo. In the present study, we have developed a stress-free sampling system, in the chronically catheterized adult guinea-pig, that has allowed us to investigate basal and activated adrenocortical activity. Indwelling carotid artery and jugular vein catheters were surgically implanted into female guinea-pigs (n = 5). Each animal was treated with vehicle, human CRH (0·2 or 2 ìg kg¢) and ACTH1-24 (0·2 or 2 ìg kg¢), and serial plasma samples removed for analysis of ACTH and cortisol concentrations by radioimmunoassay. There was no effect of serial sampling on pituitary-adrenocortical activity, indicating that the animals remain in an unstressed state. Basal plasma ACTH and cortisol concentrations were 703·9 ± 24·5 pg ml¢ and 117·9 ± 5·2 ng ml¢, respectively. Both CRH and ACTH significantly increased adrenocortical activity in a dose-dependent manner. ACTH (2 ìg kg¢) was the most potent activator leading to plasma cortisol concentrations of 647 ± 116 ng ml¢. In conclusion, we have shown that basal plasma cortisol concentrations in the guinea-pig are low compared to those obtained in previous studies by cardiac puncture or following decapitation. However, plasma ACTH concentrations are high compared to other species. We have also shown that human CRH and ACTH1-24 act as potent activators of the guinea-pig pituitary-adrenocortical axis,

Prenatal depression restricts fetal growth

“…For example, elevated prenatal maternal cortisol may affect fetal growth by both directly reaching the fetus and by changing the placental environment. From 10% to 20% of maternal cortisol can readily cross the placenta(34, 35), where it has been shown to stimulate the fetal HPA axis(34, 36) resulting in elevated fetal cortisol levels which may in turn affect fetal growth by dysregulating fetal autonomic nervous system activity(37) and mobilizing fetal energy stores via glycogenolysis (the conversion of glycogen to glucose) resulting in a high degree of calorie expenditure. Alternatively, elevated maternal cortisol, which has been shown to induce vascular constriction(38, 39) and potentiate norepinephrine-induced uterine artery contractions during mid-pregnancy(40), may also lead to reduced uterine artery blood flow, which has been associated with the development of perinatal complications including fetal growth restriction(41) (37) and premature delivery(42) possibly as a result of placental hypoxia and the restriction of oxygen and nutrient delivery to the fetus.…”

Hypothalamic–pituitary–adrenal (HPA) axis function in the California mouse (Peromyscus californicus): Changes in baseline activity, reactivity, and fecal excretion of glucocorticoids across the diurnal cycle

“…In an attempt to maximize adrenal response we chose a dose of ACTH that has been used in rats [100 µg/kg; 2, 56] but is typically higher than doses used in other species [2 µg/kg in guinea pigs, 51, 59; 0.0075 or 0.015 µg (total) in rats, 22; 10 µg/kg in marmosets, 71]. ACTH at a dose of 100 µg/kg produced a marked increase in plasma CORT 1 h following a morning (0900h) injection, when compared to saline injection.…”

Testosterone is involved in mediating the effects of prenatal stress in male guinea pig offspring

“…On PND 80, catheters were surgically implanted in the carotid artery and attached to a swivel system (Lomir Biomedical Inc., Notre‐Dame‐de‐I’lle‐Perot, PQ, Canada) above the cage, as described previously (Liu & Matthews, 1999). This allowed full rotation of the catheter and unrestricted movement of the guinea pig.…”