AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 3 589-R599, Copyright © 1991 by American Physiological Society
Nicotinic- and muscarinic-evoked release of canine adrenal catecholamines and peptides
S. L. Chritton, M. K. Dousa, T. L. Yaksh and G. M. Tyce
Department of Physiology, Mayo Clinic, Rochester, Minnesota 55905.
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.
