Abstract
1. Adrenal responses to intra-aortic infusions of acetylcholine (4.5 nmol min-1 kg-1 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-1 kg-1, 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-1). 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-1 kg-1. The increase in cortisol output appears to be secondary to an 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.