Role of calcium channels and adenylate cyclase in the PACAP-induced adrenal catecholamine secretion

Yasuo Fukushima, Takahiro Nagayama, Hisako Kawashima, Hirohiko Hikichi, Makoto Yoshida, Mizue Suzuki-Kusaba, Hiroaki Hisa, Tomohiko Kimura, Susumu Satoh

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)


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 co-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.

Original languageEnglish
Pages (from-to)R495-R501
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number2 50-2
Publication statusPublished - 2001


  • Nifedipine
  • Pituitary adenylate cyclase-activating polypeptide
  • ω-conotoxin GVIA
  • ω-conotoxin MVIIC; MDL-12330A

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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