Adrenocortical Sensitivity to Adrenocorticotropin (ACTH) in Awake Dogs Changes as a Function of the Time of Observation and after Hemorrhage Independently of Changes in ACTH

SUMMARY1. Right adrenal and various cardiovascular responses to stimulation of the peripheral end of the right splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min' kg-'). The adrenal-clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-4 days previously.2. The i.v. infusion of ACTHl-24 increased mean plasma ACTH concentration by about 1200 pg/ml and mean right adrenal cortisol output by about 500 ng minm kg-'. Stimulation of the peripheral end of the right splanchnic nerve at 4 Hz for 10 min produced a further rise in cortisol output, amounting to about 400 ng min-kg-' (P < 0-0 1). These changes in output were reflected accurately-by changes in peripheral plasma cortisol concentration.3. Closely similar amounts of adrenaline were released in response to splanchnic nerve stimulation in the presence and absence of exogenous ACTH. In the presence of ACTH the average mean output of noradrenaline (58+2 ng min-' kg-') was significantly less than that of adrenaline (102 + 4 ng min' kg-'; P < 0-001), whereas the corresponding values were not significantly different in the absence of ACTH.4. These results also confirm the fact that the fall in adrenal vascular resistance which occurs during splanchnic nerve stimulation is substantially reduced by ACTH, as is the rise in met5-enkephalin output.5. It is concluded that the splanchnic innervation is capable of enhancing the secretion of adrenal glucocorticoids in response to ACTH under physiological conditions in the conscious calf.

Section: Introductionmentioning

confidence: 68%

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

Edwards¹,

Jones²

1987

“…These include the finding that there are diurnal variations in the sensitivity of adrenal cortical cells to ACTH which cannot be related directly to changes in plasma ACTH concentration (Engeland, Byrnes, Presnell & Grann, 1981;Wood, Shinsako & Dallman, 1982a;Wood, Shinsako, Keil, Ramsay & Dallman, 1982b;Dempsher & Gann, 1983;Engeland, Lilly & Gann, 1985). Studies of adrenal cortical responses to moderate haemorrhage in the dog, have provided evidence that haemorrhage sensitizes the adrenal cortex to ACTH via a pathway which requires an intact innervation (Engeland et al 1981;Wood et al 1982a, b;Dempsher & Gann, 1983). There is also substantial evidence implicating the adrenal innervation in the phenomenon of compensatory growth that is observed in the adrenal cortex of the surviving gland following unilateral adrenalectomy or like procedures (Dallman, Engeland & Shinsako, 1976;Kleitman & Holzwarth, 1985 a, b).…”

Section: Discussionmentioning

confidence: 99%

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

Edwards

Jones

1987

SUMMARY1. Adrenal cortical responses to adrenocorticotrophin (ACTH) in conscious 2-6-week-old calves, in which both splanchnic nerves had been cut at least 7 days previously, were compared with those of normal calves of the same age in order to discover whether splanchnic nerve section affects the sensitivity of the adrenal cortex to the trophin.2. In one series of experiments an increase in the release of endogenous ACTH was elicited by an i.v. infusion of noradrenaline (333 ng min-' kg-' for 10 min) and in another the concentration of ACTH in the plasma was artificially increased by infusing synthetic ACTH1l24 intravenously at either 5 or 10 ng min-' kg-' for 10 min.3. In all groups mean plasma ACTH was linearly related to mean plasma cortisol and the sensitivity of the adrenal steroidogenic response to ACTH was found to be substantially reduced 7 or more days after section of both splanchnic nerves.

“…1979;Kaneko et al 1981;Engeland et al 1981;Wilkinson et al 1982), it has yet to be established whether changes in cortisol output that occur over much shorter periods can be caused by mechanisms other than those involving variations in plasma ACTH. Corticosteroid responses to mild haemorrhage have been reported where there is little or no change in plasma ACTH concentration (Engeland, Lilly & Gann, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…The anatomical & McBride, 1977;Krieger, 1979;Kaneko et al 1981;Engeland et al 1981;Wilkinson, Shinsako & Dallman, 1982). A potential candidate for such a role, possibly acting entirely within the gland, is met-enkephalin, an analogue of which has been shown to reduce the response to ACTH of rat adrenal cortical cells in vitro (Guaza, 1984).…”

Section: Introductionmentioning

confidence: 99%

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Edwards¹,

Hansell²,

Jones³

1986

SUMMARY1. Right medullary and various cardiovascular responses to stimulation of the peripheral end of the splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1 24, (5 ng min-kg-'). The adrenal-clamp technique was employed in conscious calves, after the pituitary stalk had been cauterized and they had recovered from anaesthesia.2. The intravenous infusion ofACTH1 24increased the plasma ACTH concentration by about 1100 pg ml-' and right adrenal venous output of cortisol by about 400 ng min' kg body weight-'. Stimulation of the splanchnic nerve at 4 Hz for 10 min had no effect on either arterial plasma ACTH concentration or the adrenal output of cortisol.3. Closely similar amounts of both adrenaline and noradrenaline were released in response to nerve stimulation in the presence and absence of exogenous ACTH. In contrast, the fall in adrenal vascular resistance of about 40 %, which normally occurred in response to splanchnic nerve stimulation, was completely abolished by ACTH.4. The adrenal produced relatively large quantities of met-enkephalin-containing peptides. During splanchnic nerve stimulation the output of these increased 20-100-fold, at which time free met5-enkephalin accounted for only 10-20 o of total. During ACTH infusion the output of free met5-enkephalin was reduced at rest and during nerve stimulation, but that of total met-enkephalin-containing peptides was unaffected. These results indicate that ACTH or an adrenal steroid may alter the processing of proenkephalin in the adrenal medulla acutely but not total opiate secretion. Alternatively, the presence ofACTH could act by influencing the population of chromaffin cells activated by splanchnic nerve stimulation.