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Am J Physiol Regul Integr Comp Physiol 281: R495-R501, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 2, R495-R501, August 2001

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

Yasuo Fukushima1, Takahiro Nagayama1, Hisako Kawashima1, Hirohiko Hikichi1, Makoto Yoshida1, Mizue Suzuki-Kusaba1, Hiroaki Hisa1, Tomohiko Kimura2, and Susumu Satoh1

1 Laboratory of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578; and 2 Department of Dental Pharmacology, The Nippon Dental University School of Dentistry at Niigata, Niigata 951-8580, Japan

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 omega -conotoxin GVIA, an N-type VDCC blocker, or omega -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.

pituitary adenylate cyclase-activating polypeptide; nifedipine; omega -conotoxin GVIA; omega -conotoxin MVIIC; MDL-12330A


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