The effect of splanchnic nerve section on the sensitivity of the adrenal cortex to adrenocorticotrophin in the calf.

Edwards, A V; Jones, C. T.

doi:10.1113/jphysiol.1987.sp016683

Cited by 57 publications

(34 citation statements)

References 20 publications

(20 reference statements)

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“…This concept of adrenal cortical control by adrenal nerves is similar to that demonstrated by Edwards and coworkers (14,15). In the fetal sheep, it is possible that the splanchnic innervation of the adrenal cortex dynamically regulates adrenal sensitivity to ACTH.…”

Section: Discussionsupporting

confidence: 73%

Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus

Wood¹,

Fraites²,

Keller‐Wood³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Wood CE, Powers Fraites M, Keller-Wood M. Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus. Am J Physiol Regul Integr Comp Physiol 296: R1813-R1819, 2009. First published March 18, 2009 doi:10.1152/ajpregu.90917.2008.-Decreases in fetal blood pressure stimulate homeostatic stress responses that help return blood pressure to normal levels. Fetal hypothalamus-pituitary-adrenal (HPA) axis responses to hypotension are mediated by chemoreceptor and baroreceptor reflexes and ischemia of the fetal central nervous system. Indomethacin, a nonselective inhibitor of prostaglandin endoperoxide synthase (PGHS)-1 and -2, attenuates the HPA response to hypotension in the fetus. The present study was designed to test the hypothesis that selective inhibition of PGHS-2 also inhibits the HPA response to cerebral hypoperfusion. We studied 13 chronically catheterized fetal sheep (126 -136 days gestation). Five fetal sheep were subjected to intracerebroventricular infusion of nimesulide (0.01 mg/ day), a specific inhibitor of PGHS-2, and eight were treated with vehicle (DMSO in water) for 5 days. Each fetus was subjected to a 10-min period of brachiocephalic occlusion, which decreased carotid arterial pressure ϳ75% and reflexively increased fetal plasma concentrations of ACTH, POMC, cortisol, and femoral arterial pressure, and decreased fetal heart rate. Nimesulide significantly inhibited the ACTH response to the BCO, while significantly augmenting the reflex cardiovascular response and altering fetal heart rate variability consistent with increased sympathetic nervous system activity. The results of this study demonstrate that the activity of PGHS-2 in the brain is a necessary component of the fetal HPA response to cerebral hypoperfusion in the late-gestation fetal sheep. These results are consistent with those of recent study, in which we demonstrated that the preparturient increase in fetal ACTH secretion depends upon PGHS-2 activity within the fetal brain. adrenocorticotropin; cortisol; fetus; blood pressure EICOSANOIDS HAVE BEEN LONG recognized for their importance as signaling molecules in the fetus (7). Plasma concentrations of PGE 2 are much higher in the late-gestation fetus than in the postnatal animal (7), and the concentrations increase prior to normal parturition in this species. The pattern of increase of fetal plasma PGE 2 , combined with the observation that exogenous PGE 2 stimulates fetal hypothalamus-pituitary-adrenal (HPA) axis activity (7), led to the hypothesis that PGE 2 secreted by the placenta acts as a hormone to stimulate fetal HPA axis activity prior to spontaneous parturition (34). Although the endogenous plasma concentrations of PGE 2 are high compared with plasma concentrations postnatally, intracarotid arterial infusion of PGE 2 , producing plasma concentrations within the range of that occur endogenously prior to spontaneous parturition, failed to increase fetal HPA axis activity (11). From the results of that study, we conclude...

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Section: Discussionsupporting

confidence: 73%

Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus

Wood¹,

Fraites²,

Keller‐Wood³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Only relatively recently has the importance of the innervation of the gland on adrenocortical secretion been determined. Thus, Edwards and Jones (38) using conscious, hypophysectomized calves showed that stimulation of the splanchnic input to the adrenal gland doubled, whereas splanchnic denervation halved (39), the output of cortisol in response to an exogenous infusion of ACTH. In the fetus, similar neural mechanisms operate in the control of stimulated adrenocortical secretion, because functional innervation of the ovine fetal adrenal gland is present by the final third of gestation (40,41), and Myers et al (42) showed that splanchnic nerve section in the ovine fetus had no effect on basal plasma cortisol concentration but significantly attenuated the cortisol increment during acute hypotensive stress.…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in the Ovine Fetal Cortisol Response to Stress

2011

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This study tested the hypothesis that the sexually dimorphic adrenocortical response to stress is already established before birth. Chronically instrumented late gestation pregnant sheep carrying 16 male and 15 female age-matched singleton fetuses were subjected to an acute episode of hypoxic stress. Maternal and fetal blood gases, adrenocorticotrophic hormone (ACTH), and cortisol were measured. In addition, six male and six female fetuses received the ACTH analog, Synacthen, and plasma cortisol was measured. During hypoxic stress, the increment in plasma cortisol was 2-fold greater in male versus females fetuses (30.6 Ϯ 3.2 versus 14.3 Ϯ 2.0 ng/mL; p Ͻ 0.001) mediated, in part, by greater adrenocortical sensitivity to ACTH. The data support the hypothesis tested and show that sex-specific differences in the cortisol stress response are present before birth with the output of cortisol being much greater in male than in female fetuses. (Pediatr Res 69: 118-122, 2011) D uring threatening situations, the stress system coordinates adaptive responses that adjust homeostatic mechanisms to increase the individual's chance of survival. The hypothalamic-pituitary-adrenal (HPA) axis constitutes one of the main efferent limbs of the stress system, and measurement of circulating plasma adrenocorticotrophic hormone (ACTH) and cortisol concentrations are established measures of the level of psychological, social, and/or physiological stress (1). An adequate capacity for secretion of adrenal glucocorticoids is essential for fetal development and maintenance of an independent life (2,3); the adrenal glands are thus highly perfused with blood and richly innervated. Adrenocortical secretion of glucocorticoids is often used as an example of classical endocrinology, with the principal control provided by the release of ACTH from the distant anterior pituitary and with excess cortisol production switching off the stimulatory signal through negative feedback.It is widely acknowledged that there are differences in the response to stress between the sexes, but the reason underlying these differences is unclear. The literature is often contradictory due, in part, to variations in the type of stress imposed, the particular species being studied, and the age of the subject. For example, in adult rats, females have greater stress responses (4,5); however, in humans, it is young men and old women who show an increased stress response relative to old men and young women (6). In addition, when compared with agematched women, men showed consistently higher plasma cortisol responses to stress in four independent studies (7). It is also accepted that sex hormones can alter the magnitude of the stress response, with androgens being suppressive and estrogens being stimulatory to the HPA axis (8,9) and that manipulation of gonadal steroids soon after birth can have activational and organizational effects on the function of the stress axis later in life (9). Development of the fetal HPA axis is exquisitely controlled and critical for the a...

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“…Accordingly, the greatly increased fat deposition in TG animals (after the age of 4 months), especially accumulated in adipose tissue (Pepin et al, 1992a), may be attributable to the decreased sympathetic nervous activity rather than to GR dysf unction. Because sympathetic activity enhances ACTH-dependent cort secretion from the adrenal gland (Edwards and Jones, 1987;Engeland and Gann, 1989;Bornstein et al, 1990;Jasper and Engeland, 1994;Dijkstra et al, 1996), the decreased sensitivity of the adrenal gland for ACTH may be a consequence of the reduced sympathetic outflow in TG mice. Thus, it is important to note that the phenotype of the GR defunct mice appears for a large part to be determined by the reduced hypothalamic CRH activity.…”

Section: Discussionmentioning

confidence: 99%

Reduced Activity of Hypothalamic Corticotropin-Releasing Hormone Neurons in Transgenic Mice with Impaired Glucocorticoid Receptor Function

et al. 1998

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Loss of central glucocorticoid receptor (GR) function is thought to be involved in the development of neuroendocrine and psychiatric disorders associated with corticotropin-releasing hormone (CRH) hyperactivity. The possible causal relationship between defective GR function and altered activity of CRH neurons was studied in transgenic mice (TG) expressing antisense RNA against GR. Immunocytochemical studies showed significant reductions in CRH immunoreactive neurons in the paraventricular nucleus (PVN) and in CRH and vasopressin (AVP) stores in the external zone of the median eminence. Concomitantly, stimulus-evoked CRH secretion from mediobasal hypothalami of TG mice in vitro was reduced significantly. However, CRH mRNA levels in the PVN of TG mice were marginally lower than those in wild-type (WT) mice.125 I-CRH binding autoradiography revealed no differences between WT and TG animals in any of the brain regions that were studied. Basal plasma corticosterone (cort) levels and 125 I-CRH binding, CRH-R 1 mRNA, POMC mRNA, and POMC hnRNA levels in the anterior pituitary gland were similar in WT and TG mice. Intraperitoneal injection of interleukin-1␤ (IL-1␤) increased plasma cort levels, CRH mRNA in the PVN, and anterior pituitary POMC hnRNA similarly in WT and TG mice. The injection of saline significantly reduced anterior pituitary CRH-R 1 mRNA levels in WT mice, but not in TG mice, whereas IL-1␤ produced a decrease in these mRNA levels in both strains.The data show that long-term GR dysfunction can be associated with reduced activity of CRH neurons in the PVN and decreased sensitivity of pituitary CRH-R 1 mRNA to stimulusinduced downregulation. Moreover, the hypothalamic changes observed in this model suggest that impaired GR function, at least if present since early embryonic life, does not necessarily result in CRH hyperexpression characteristics of disorders such as major depression.

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The effect of splanchnic nerve section on the sensitivity of the adrenal cortex to adrenocorticotrophin in the calf.

Cited by 57 publications

References 20 publications

Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus

Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus

Sex Differences in the Ovine Fetal Cortisol Response to Stress

Reduced Activity of Hypothalamic Corticotropin-Releasing Hormone Neurons in Transgenic Mice with Impaired Glucocorticoid Receptor Function

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