Nicotinic- and muscarinic-evoked release of canine adrenal catecholamines and peptides

Abstract

The tissue content and overflow of norepinephrine (NE), epinephrine (Epi), dopamine (DA), Met-enkephalin (Met-Enk), and neuropeptide Y (NPY) from isolated, retrogradely perfused dog adrenal glands were studied. Under resting conditions, approximately 25% of the overflow of autocoids from the glands was Ca2+ dependent; the cholinergic antagonists hexamethonium and atropine had no effects on basal efflux. Stimulation with the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP; 3 or 50 microM) or with the muscarinic agonist pilocarpine (50 microM or 1 mM) evoked releases of autocoids. These releases were blocked or dramatically reduced by appropriate antagonists or by the removal of Ca2+ from the perfusate. Expressed as percentages of tissue stores, the rank order of overflow of autocoids was E approximately DA much greater than NE during resting conditions, DA much greater than E approximately NE during stimulation with 50 microM DMPP, and DA greater than Epi greater than NE during stimulation with 1 mM pilocarpine. These data are consistent with different mechanisms of release for the catecholamines, perhaps from different cell populations. The data support corelease of peptides and catecholamines, although clear pairing of autocoids could not be confirmed.

Endogenous opioids suppress activation of nociceptors by sub‐nanomolar nicotine

“…Adrenal denervation also uncovered this nicotine‐induced action and occluded enhancement by naloxone, suggesting that the naloxone‐sensitive inhibition of nicotinic receptors is mediated by endogenous opioids derived from the adrenal medulla. Supported by the reports that denervation of the adrenal medulla is known to result in a decrease in circulating opioids ( Przewlocka et al ., 1986 ; Mason et al ., 1987 ; Chritton et al ., 1991 ), our results provide evidence that endogenous release of opioids exert a tonic inhibitory action on the proinflammatory effect of low‐dose nicotine. Because both opioid receptors ( Taddese et al ., 1995 ; Ma et al ., 1997 ) and nicotinic receptors ( Steen & Reeh, 1993 ; Boyd et al ., 1991 ) are present on sensory neurons, it is likely that the actions we observed are mediated by interaction between receptors located on primary afferent nerve endings in the knee joint.…”

Characterization of cerebral microvasculature in transgenic mice with endothelium targeted over-expression of GTP-cyclohydrolase I

“…Plasma samples were stored at −80°C until assayed. Samples were absorbed onto activated alumina at pH 8.6, washed and eluted with diluted acetic acid as described (Chritton et al, 1991). Norepinephrine, epinephrine and dopamine were determined from elutes by HPLC and electrochemical detection.…”