In:
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 2 ( 2001-08-01), p. R495-R501
Abstract:
We elucidated the functional contribution of voltage-dependent calcium channels (VDCCs) and adenylate cyclase to epinephrine (Epi) and norepinephrine (NE) secretion induced by pituitary adenylate cyclase-activating polypeptide (PACAP) in the isolated perfused rat adrenal gland. PACAP increased Epi and NE output, which was inhibited by perfusion with calcium-free solution or by nifedipine, an L-type VDCC blocker. However, the PACAP-induced responses were resistant to ω-conotoxin GVIA, an N-type VDCC blocker, or ω-conotoxin MVIIC, a P/Q-type VDCC blocker. MDL-12330A, an adenylate cyclase inhibitor, inhibited the PACAP-induced increase in Epi, but not NE, output. Treatment with nifedipine and MDL-12330A caused additive inhibition of the PACAP-induced catecholamine responses. These results suggest that opening of L-type VDCCs is responsible for adrenal catecholamine secretion induced by PACAP and that activation of adenylate cyclase is involved in the PACAP-induced Epi, but not NE, secretion. These pathways may act independently of each other.
Type of Medium:
Online Resource
ISSN:
0363-6119
,
1522-1490
DOI:
10.1152/ajpregu.2001.281.2.R495
Language:
English
Publisher:
American Physiological Society
Publication Date:
2001
detail.hit.zdb_id:
1477297-8
SSG:
12
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