| Abstrakt: |
An in-situ isolated rat adrenal perfusion technique has been devised to study the opioid control of neurally mediated adrenomedullary catecholamine release. Adrenomedullary catecholamine secretion was induced by electrical stimulation of the cut end of the left descending thoracic sympathetic chain on platinum electrodes. The half-maximal stimulatory potential (ED50) of the system was 8 V, 20 Hz, with 300μs pulse width. Basal release of catecholamine from the adrenal was constant using a perfusion flow rate of 100–300μl/min, but increased significantly with increasing perfusion temperature over the range 36–38 °C. Following repetitive 30-s stimulation of the left thoracic sympathetic chain, and 3-min fraction collections, the total amount of catecholamine released per fraction remained within 80–100% of the maximum release for up to eight consecutive stimuli. The release of catecholamines was completely blocked by hexamethonium (0·1 mmol/l), but recovered to preblockade values within two further stimuli. Using the ED50and the first three stimuli as control, the effects of morphine (10 nmol/l–1 mmol/l), d-Ala2-MePhe4-Met-enkephalin-(O5)-ol (DAMME; 10 nmol/l–0·1 mmol/l) and naloxone (10 nmol/l– 10 μmol/l) on the response to the next three stimuli were compared. Morphine, DAMME or naloxone did not significantly alter the amount of catecholamine released by this form of stimulation. Therefore in the rat, under the conditions used, there is no evidence for mu (μ) or delta (†) opiate modulation of neurally mediated catecholamine release from the rat adrenal medulla.J. Endocr.(1986) 111,7–15 |
