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1 Department of Medical Physiology, The Panum Institute, University of Copenhagen DK 2200; 2 Department of Clinical Biochemistry, Bispebjerg Hospital DK 2400; and 3 Department of Clinical Biochemistry, Rigshospitalet, DK 2100 Copenhagen, Denmark
The concentration of pituitary adenylyl cyclase-activating
polypeptide [PACAP-(1-38)] in porcine adrenal glands amounted to
14 ± 3 pmol/g tissue. PACAP immunoreactive (PACAP-IR) fibers innervated adrenal chromaffin cells (often co-localized with choline acetyltransferase). Subcapsular fibers traversed the cortex-innervating endocrine cells and blood vessels [some co-storing mainly calcitonin gene-related peptide but also vasoactive intestinal polypeptide (VIP)]. PACAP-IR fibers were demonstrated in the splanchnic nerves, whereas IR adrenal nerve cell bodies were absent. In isolated, vascularly perfused adrenal gland, splanchnic nerve stimulation (16 Hz)
and capsaicin (10
5 M) increased PACAP-(1-38) release
(1.6-fold and 6-fold respectively, P = 0.02).
PACAP-(1-38) dose-dependently stimulated cortisol (2 × 10
10 M; 24-fold increase, P = 0.02) and
chromogranin A fragment (2 × 10
9 M; 15-fold
increase, P = 0.05) secretion. Both were strongly inhibited by the PAC1/VPAC2 receptor antagonist
PACAP-(6-38) (10
7 M). PACAP-(6-38) also
inhibited splanchnic nerve (10 Hz)-induced cortisol secretion but
lacked any effect on splanchnic nerve-induced pancreastatin secretion.
PACAP-(1-38) (2 × 10
10 M) decreased vascular
resistance from 5.5 ± 0.6 to 4.6 ± 0.4 mmHg · min · ml
1. PACAP-(6-38) had
no effect on this response. We conclude that PACAP-(1-38) may play
a role in splanchnic nerve-induced adrenal secretion and in afferent
reflex pathways.
pituitary adenylyl cyclase-activating polypeptide receptor antagonist; pancreastatin; catecholamines; cortisol
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