The effect of splanchnic nerve stimulation on adrenocortical activity in conscious calves.

Edwards, A V; Jones, C. T.

doi:10.1113/jphysiol.1987.sp016373

Cited by 97 publications

(56 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One such is the innervation to the gland, which exerts an important modulating influence (Engeland, A. V. EDWARDS AND C. T. JONES Byrnes, Presnell, & Gann, 1981;Wood, Shinsako & Dallman, 1982a;Wood, Shinsako, Keil, Ramsay & Dallman, 1982b;Dempsher & Gann, 1983;Engeland, Lilly & Gann, 1985;Edwards, Jones & Bloom, 1986). More recently it has been established that splanchnic nerve stimulation enhances the steroidogenic response of the adrenal cortex to ACTH (Edwards & Jones, 1987).…”

Section: Introductionmentioning

confidence: 99%

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Edwards¹,

Jones²

1988

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

SUMMARY1. The output of corticotrophin releasing factor-like immunoreactivity (CRF) from the adrenal gland has been investigated using the 'adrenal clamp' technique in conscious calves.2. Stimulation of the peripheral end of the splanchnic nerve for 10 min increased the mean output of CRF progressively, so that it had risen by about twentyfold, to a peak incremental value of 24 +4 pmol min-' kg-' at 10 min. This response was significantly increased by stimulating in bursts at 40 Hz for 1 s at 10 s intervals, which raised the mean CRF output by 44+7 pmol min-' kg-' at 10 min (P < 0-05).3. The mean output of adrenaline and noradrenaline rose more abruptly in response to splanchnic nerve stimulation with peak incremental values realized within 2-5 min. However, the ratios of adrenal CRF to catecholamine output were closely similar during the later stages of stimulation (7-5-10 min). There was a similarly abrupt rise in adrenal cortisol output in response to splanchnic nerve stimulation which was, nevertheless, linearly related to arterial plasma ACTH concentration throughout.4. In hypophysectomized calves, administration of adrenocorticotrophic hormone (ACTH1-24) at a dose of 5 ng min-' kg-1 reduced the output of adrenal CRF in response to splanchnic nerve stimulation by about 50% (P < 0 05). 5. CRF isolated from adrenal venous effluent plasma, collected both at rest and during splanchnic nerve stimulation, was separated by reverse-phase high-pressure liquid chromatography and found to elute in a position identical to that of human 41CRF. This suggests that adrenal CRF is structurally closely similar to its pituitary counterpart.

show abstract

Section: Introductionmentioning

confidence: 99%

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Edwards¹,

Jones²

1988

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…[Met5]-enkephalin was measured by a specific radioimmunoassay as described previously (Edwards, Hansell & Jones, 1986;Edwards & Jones, 1987 …”

Section: Experiments Proceduresmentioning

confidence: 99%

Muscarinic adrenal responses to acetylcholine in conscious calves.

Jones

Edwards

1991

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

SUMMARY1. Adrenal responses to intra-aortic infusions of acetylcholine (4-5 nmol min-' kg-' for 10 min) have been investigated in hypophysectomized conscious calves given exogenous adrenocorticotrophic hormone (ACTH) (2 ng min-' kg-' i.v.) in the presence and absence of hexamethonium.2. Acetylcholine produced a significant increase in adrenal cortisol output and plasma cortisol concentration. In the absence of nicotinic blockade with hexamethonium this was apparently accounted for by an increase in adrenal ACTH presentation secondary to increased adrenal blood flow. However, administration of hexamethonium revealed a direct steroidogenic action of acetylcholine in the presence of exogenous ACTH 3. Adrenal medullary responses to acetylcholine, including the release of catecholamines, enkephalins and corticotrophin-releasing factor (CRF), were not significantly reduced by nicotinic blockade.4. It is concluded that both adrenal medullary and cortical responses to intraaortic infusions of acetylcholine at a low dose are mediated mainly by muscarinic receptors, as it has previously been shown that they are substantially reduced in the presence of atropine.

show abstract

“…In addition, although it is known that the ovine placenta is not permeable to ACTH (43) and that maternal cortisol is metabolized in the placenta by the enzyme 11 ␤-hydroxysteroid dehydrogenase (44), the absence of any significant alterations in maternal plasma ACTH and cortisol Previous studies have suggested a role for the splanchnic sympathetic nerves innervating the adrenal gland in the steroidogenic response to stress, because stimulation of the splanchnic nerves doubled and section of these nerves halved the increase in plasma concentrations of cortisol in response to exogenous ACTH in conscious, hypophysectomized calves (45,46) and lambs (47). Similarly, the increase in plasma concentrations of cortisol in response to acute hypoxemia were attenuated or completely abolished in carotid chemodenervated sheep (33) and llama (48) fetuses, respectively.…”

Section: Dexamethasone and The Materno-fetal Hpa Axismentioning

confidence: 99%

Pituitary-Adrenal Responses to Acute Hypoxemia During and After Maternal Dexamethasone Treatment in Sheep

et al. 2004

View full text Add to dashboard Cite

The effects of maternal dexamethasone treatment on hypothalamic-pituitary-adrenal axis function were determined during basal and hypoxemic conditions in maternal and fetal sheep. Under halothane, ewes and their fetuses were catheterized at 117 d gestation (term ϭ 145 d). Starting at 124 d, the ewes received i.m. injections of two doses of either dexamethasone (12 mg) or saline at 24-h intervals. All animals experienced one episode of hypoxemia when the dexamethasone was present in the maternal and fetal circulations [125 Ϯ 1 d (H1)] and a second episode of hypoxemia when the steroid was no longer detectable in either the maternal or fetal circulations [128 Ϯ 1 d (H2)]. The fall in partial pressure of oxygen in arterial blood in response to hypoxia was similar in the two episodes in both the fetal and the maternal blood. Maternal dexamethasone treatment diminished maternal and fetal basal plasma cortisol but not ACTH during the normoxic period of H1 but not H2. In control animals, hypoxemia induced increases in fetal but not maternal ACTH and cortisol concentrations. In dexamethasone-treated animals, maternal ACTH and cortisol concentrations also remained unchanged from baseline in both H1 and H2. In contrast, fetal plasma ACTH and cortisol responses to hypoxemia were significantly suppressed during H1 but not H2. Correlation of fetal plasma ACTH and cortisol concentrations suggested diminished cortisol output without a change in adrenocortical responsiveness in dexamethasone-treated fetuses during H1 but not H2. Since the pioneering discovery of Liggins (1) that glucocorticoids are essential for the maturation of fetal systems in preparation for extrauterine life, synthetic glucocorticoids, such as dexamethasone, have been used routinely in human clinical practice to treat pregnant women who are at risk of preterm delivery (2-4). Such prophylactic treatment mimics the normal prepartum increase in endogenous cortisol output by the fetal adrenal that switches tissue accretion to differentiation (5). Antenatal glucocorticoid treatment has resulted in significant decreases in the incidence of respiratory distress syndrome, necrotizing enterocolitis, intraventricular hemorrhage, and neonatal mortality associated with preterm birth (3,6).Despite the clear benefits of antenatal glucocorticoid therapy, concerns have been expressed about the safety of the current dosing regimen, in particular with regards to maternal and fetal adrenal suppression resulting from negative feedback by the synthetic steroid (4). In addition, the effects of synthetic glucocorticoids on the fetal defense responses to hypoxemic insults have been identified by the National Institutes of Health in the United States as an area of research needed to guide intrapartum clinical care (4). This is important for two reasons. First, the ovine hypothalamic-pituitary-adrenal (HPA) axis is activated in response to acute hypoxemia in the mother and the fetus and plays an integral role in the fetal defense response to acute hypoxemia (7). Second, episodes of ...

show abstract

The effect of splanchnic nerve stimulation on adrenocortical activity in conscious calves.

Cited by 97 publications

References 22 publications

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Muscarinic adrenal responses to acetylcholine in conscious calves.

Pituitary-Adrenal Responses to Acute Hypoxemia During and After Maternal Dexamethasone Treatment in Sheep

Contact Info

Product

Resources

About