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

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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.

Section: Discussionmentioning

confidence: 99%

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

Edwards¹,

Jones²

1988

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“…Preparatory surgery involved two successive operations at intervals of 3-4 days. On the first occasion the pituitary stalk and the contents of the sella turcica were cauterized as described previously (Edwards, Hansell & Jones, 1986) and narrowbore polytetrafluoroethylene (Teflon) catheters were inserted into the saphenous arteries so that the tip of one lay in the lower thoracic aorta with the other in the abdominal aorta. These were used subsequently to monitor aortic blood pressure and heart rate and for collection of arterial blood samples.…”

Section: Methodsmentioning

confidence: 99%

Endocrine responses to intra‐aortic infusions of acetylcholine in conscious calves.

Jones

Edwards

Bloom

1991

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SUMMARY1. Adrenal responses to intra-aortic infusions of acetylcholine (4 5 nmol min-' kg-' for 10 min) have been investigated in conscious, functionally hypophysectomized, 3-to 6-week-old calves, in the presence and absence of exogenous ACTH (2 ng min-' kg-, i.v.).2. Acetylcholine produced a substantial fall in adrenal vascular resistance, which was significantly reduced in the presence of exogenous ACTH, while producing minimal changes in aortic blood pressure and heart rate.3. There was also a significant rise in right adrenal cortisol output which was sufficient to produce a measurable rise in plasma cortisol concentration. The effect could be accounted for by the increase in adrenal ACTH presentation. It was abolished by pre-treatment with atropine (0-2 mg kg-'). A small but significant rise in aldosterone output during acetylcholine infusions was also abolished in the presence of ACTH.4. Both adrenaline and noradrenaline were released during intra-aortic acetylcholine infusions and these responses were substantially reduced, but not abolished, by pre-treatment with atropine.5. Acetylcholine also stimulated the release of corticotrophin-releasing factor (CRF) and [Met5]enkephalins from the gland. The output of CRF was enhanced and that of free [Met5]enkephalin was significantly reduced in the presence of exogenous ACTH. All these responses were largely, but not completely, suppressed by atropine.6. Acetylcholine also promoted the release of the pancreatic hormones glucagon, insulin and pancreatic polypeptide (PP). The amounts of pancreatic glucagon and insulin that were released were highly dependent on the concentration of glucose in the circulating plasma and all these responses were abolished by atropine.7. It is concluded that acetylcholine is capable of stimulating the release of a wide variety of agonists from the adrenal gland when infused intra-aortically at a dose of 4.5 nmol min-' kg-'. The increase in cortisol output appears to be secondary to an 16 PHY 439 C. T. JONES, A. V. EDWARDS AND S. R. BLOOM increase in blood flow whereas the adrenal medullary responses are not, and appear to be due largely, but not entirely, to activation of muscarinic receptors.

“…Kimura, Rossier. Stein & Udenfriend (1978) and bv Chamiinade et al (1984) (see Edwards et al 1986, for further details).…”

Section: Analytical Proceduresmentioning

confidence: 99%

“…Met5-enkephalin was measured by radioimmunoassay as described previously (Edwards et al 1986). The assay was carried out either on samples of untreated adrenal venous effluent plasma to provide a value for free met5-enkephalin or after proteolytic digestion to liberate met5-enkephalin from any released precursor, as a measure of total met5-enkephalin, essentially as described by Lewis.…”

Section: Analytical Proceduresmentioning

confidence: 99%

Adrenal responses to splanchnic nerve stimulation in conscious calves given naloxone.

Edwards

Jones

1989

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SUMMARY1. The effects of stimulating the peripheral end of the right splanchnic nerve in the presence of naloxone (2 mg kg-') have been investigated in conscious 3 to 6-week-old calves.2. Mean aortic blood pressure rose to significantly higher levels during splanchnic stimulation in bursts at 40 Hz for 1 s at 10 s intervals than it did during stimulation at the corresponding continuous frequency (4 Hz). Furthermore, naloxone significantly reduced the fall in mean vascular resistance in response to both patterns of stimulation.3. The output of catecholamines from the adrenal gland, together with the proportion of noradrenaline released, was significantly enhanced by stimulating the splanchnic nerves in bursts in animals pre-treated with naloxone and the proportion of noradrenaline released also increased. In both cases the output of adrenaline and noradrenaline was within the same range as that reported previously in normal control animals.4. Naloxone significantly increased the amounts of enkephalin-like immunoreactivity and corticotrophin-releasing factor (CRF)-like immunoreactivity released from the adrenal gland in response to splanchnic nerve stimulation and raised the proportion of total to free met5-enkephalin that was secreted.5. Naloxone also inhibited the rise in plasma adrenocorticotrophic hormone (ACTH) concentration during continuous stimulation at 4 Hz, but not during stimulation at 40 Hz in bursts. Under these latter conditions the output of cortisol apparently directly from the adrenal gland was inhibited. The finding that splanchnic nerve stimulation can potentiate the output of cortisol in response to ACTH was confirmed.6. These results provide evidence that release of enkephalins and of CRF from the adrenal is inhibited by activating opioid receptors within the gland itself.