TY - JOUR
T1 - Role of calcium channels and adenylate cyclase in the PACAP-induced adrenal catecholamine secretion
AU - Fukushima, Yasuo
AU - Nagayama, Takahiro
AU - Kawashima, Hisako
AU - Hikichi, Hirohiko
AU - Yoshida, Makoto
AU - Suzuki-Kusaba, Mizue
AU - Hisa, Hiroaki
AU - Kimura, Tomohiko
AU - Satoh, Susumu
PY - 2001
Y1 - 2001
N2 - 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.
AB - 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.
KW - Nifedipine
KW - Pituitary adenylate cyclase-activating polypeptide
KW - ω-conotoxin GVIA
KW - ω-conotoxin MVIIC; MDL-12330A
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U2 - 10.1152/ajpregu.2001.281.2.r495
DO - 10.1152/ajpregu.2001.281.2.r495
M3 - Article
C2 - 11448853
AN - SCOPUS:0034885732
VL - 281
SP - R495-R501
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 2 50-2
ER -