In:
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 5 ( 2001-11-01), p. R1562-R1567
Abstract:
We elucidated the contribution of endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) to neurally evoked catecholamine secretion from the isolated perfused rat adrenal gland. Infusion of PACAP (100 nM) increased adrenal epinephrine and norepinephrine output. The PACAP-induced catecholamine output responses were inhibited by the PACAP type I receptor antagonist PACAP- (6-38) (30–3,000 nM) but were resistant to the PACAP type II receptor antagonist [Lys 1 ,Pro 2,5 ,Ara 3,4 ,Tyr 6 ]-vasoactive intestinal peptide (LPAT-VIP; 30–3,000 nM). Transmural electrical stimulation (ES; 1–10 Hz) or infusion of ACh (6–200 nM) increased adrenal epinephrine and norepinephrine output. PACAP-(6–38) (3,000 nM), but not LPAT-VIP, also inhibited the ES-induced catecholamine output responses. However, PACAP-(6–38) did not affect the ACh-induced catecholamine output responses. PACAP at low concentrations (0.3–3 nM), which had no influence on catecholamine output, enhanced the ACh-induced catecholamine output responses, but not the ES-induced catecholamine output responses. These results suggest that PACAP is released from the nerve endings to facilitate the neurally evoked catecholamine secretion through PACAP type I receptors in the rat adrenal gland.
Type of Medium:
Online Resource
ISSN:
0363-6119
,
1522-1490
DOI:
10.1152/ajpregu.2001.281.5.R1562
Language:
English
Publisher:
American Physiological Society
Publication Date:
2001
detail.hit.zdb_id:
1477297-8
SSG:
12
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