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

Abstract

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.

Pancreatic endocrine responses to the peptides VIP and PACAP in the conscious calf

“…The experiments were carried out in thirteen conscious pedigree male Jersey calves 23-44 days after birth (27.5-40 (Jones, Edwards & Bloom, 1991 …”

Muscarinic adrenal responses to acetylcholine in conscious calves.

“…As shown in Table 1, adding the outputs of the catecholamines, enkephalin and of CRF obtained in the presence of the two blocking agents (present results and Jones et al 1991) produces a total which exceeds that obtained in their absence in each case (Table 1). In view of the fact that they are all substantially reduced after atropine we conclude that they are due largely, if not entirely to, activation of muscarinic receptors under these particular experimental conditions.…”

“…Quite pronounced species differences have been claimed with respect to the relative importance of the two types of receptor with nicotinic receptors believed to play the major role in mediating NV'M 9364 C. T. JONES AND A. V. EDWARDS catecholamine release in response to splanchnic nerve stimulation in the cat and dog (Douglas, 1975), the gerbil (Douglas, Kanno & Sampson, 1967) and rat (Yoshikazi, 1973) and solely responsible for doing so in the ox (Douglas, 1975); in contrast, the adrenal medulla of the chicken has been reported to secrete catecholamines solely in response to activation of muscarinic receptors (Douglas, 1975). In the conscious calf a variety of adrenal responses to acetylcholine were found to be largely, but not completely, blocked by atropine when the agonist was infused intra-aortically at the comparatively low dose of 4-5 nmol min-' kg-' (Jones, Edwards & Bloom, 1991). The possibility that these responses depend more on activation of muscarinic rather than nicotinic receptors has now been investigated by assessing them following pretreatment with hexamethonium.…”

Cholinergic regulation of the rat adrenal zona glomerulosa

“…Several groups have reported actions of acetylcholine (ACh) on adrenocortical steroid secretion in frog (Benyamina et al 1987), calf ( Jones et al 1991), bovine (Hadjian et al 1982, Kojima et al 1986, Walker et al 1990 and human (Stern et al 1989) adrenals.…”