Korean J Physiol Pharmacol.
1999 Jun;3(3):339-350.
Mechanism of pituitary adenylate cyclase-activating polypeptide-induced inhibition on catecholamine secretion evoked by cholinergic stimulation and membrane depolarization in the rat adrenal gland
- Affiliations
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- 1Department of Pharmacology, College of Medicine, Chosun University, 375 Seosuk-dong, Dong-gu, Kwangju, 501-759 South Korea.
- 2Dermatology, College of Medicine, Chosun University, Kwangiu 501-759, Korea.
Abstract
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The present study was attempted to examine the effect of pituitary
adenylate cyclase-activating polypeptide (PACAP) on catecholamine (CA)
secretion evoked by cholinergic stimulation, membrane depolarization
and calcium mobilization from the isolated perfused rat adrenal gland.
The perfusion of PACAP (10 nM) into an adrenal vein for 60 min produced
a great inhibition in CA secretion evoked by ACh (5.32 X 10(-3) M), high
K+ (5.6 X 10(-2) M), DMPP (10(-4) M for 2 min), McN-A-343 (10(-4) M for 2
min), cyclopiazonic acid (10(-5) M for 4 min) and Bay-K-8644 (10(-5) M for
4 min). Also, in the presence of neuropeptide (NPY), which is known to
be co-localized with norepinephrine in peripheral sympathetic nerves,
CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343,
Bay-K-8644 and cyclopiazonic acid were also significantly depressed.
However, in adrenal glands preloaded with PACAP (10 nM) under the
presence of VIP antagonist ((Lys1, Pro2.5, Arg3.4, Tyr6)-VIP (3 micrometer))
for 20 min, CA secretory responses evoked by ACh, high potassium, DMPP,
McN-A-343, Bay-K-8644 and cyclopiazonic acid were not altered greatly
in comparison to the case of PACAP-treatment only. Taken together,
these results suggest that PACAP causes the marked inhibition of CA
secretion evoked by stimulation of cholinergic (both nicotinic and
muscarinic) receptors as well as by membrane depolarization, indicating
that this effect may be mediated by inhibiting influx of extracellular
calcium and release in intracellular calcium in the rat adrenomedullary
chromaffin cells.