TY - JOUR
T1 - Effect of cilnidipine, a novel dihydropyridine Ca2+ channel blocker, on adrenal catecholamine secretion in anesthetized dogs
AU - Nagayama, Takahiro
AU - Yoshida, Makoto
AU - Suzuki-Kusaba, Mizue
AU - Hisa, Hiroaki
AU - Kimura, Tomohiko
AU - Satoh, Susumu
PY - 1998/9/1
Y1 - 1998/9/1
N2 - We investigated the effect of cilnidipine, a novel dihydropyridine Ca2+ channel blocker possessing blocking actions on N-type and L-type voltage-dependent Ca2+ channels (VDCCs), in comparison with the L-type VDCC blocker nifedipine, on adrenal catecholamine secretion in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. Ca2+ channel blockers and cholinergic agonists were infused and injected, respectively, into the adrenal gland through the phrenicoabdominal artery. Cilnidipine (0.3-3 μg/min) inhibited increases in both epinephrine (EPI) and norepinephrine (NE) output induced by SNS (2 Hz), ACh (1.5 μg), and DMPP (0.2 μg). However, cilnidipine inhibited increase in NE output induced by muscarine (1 μg) without affecting increase in EPI output. Nifedipine (0.3-3 μg/min) inhibited the ACh- and DMPP-induced increases in EPI and NE output without affecting the SNS- and muscarine- induced increases in EPI and NE output. From these results, it seems likely that the inhibition by cilnidipine of the SNS-induced EPI and NE secretion and of the muscarine-induced NE secretion is related to its blocking action on N-type VDCCs.
AB - We investigated the effect of cilnidipine, a novel dihydropyridine Ca2+ channel blocker possessing blocking actions on N-type and L-type voltage-dependent Ca2+ channels (VDCCs), in comparison with the L-type VDCC blocker nifedipine, on adrenal catecholamine secretion in response to splanchnic nerve stimulation (SNS), acetylcholine (ACh), the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. Ca2+ channel blockers and cholinergic agonists were infused and injected, respectively, into the adrenal gland through the phrenicoabdominal artery. Cilnidipine (0.3-3 μg/min) inhibited increases in both epinephrine (EPI) and norepinephrine (NE) output induced by SNS (2 Hz), ACh (1.5 μg), and DMPP (0.2 μg). However, cilnidipine inhibited increase in NE output induced by muscarine (1 μg) without affecting increase in EPI output. Nifedipine (0.3-3 μg/min) inhibited the ACh- and DMPP-induced increases in EPI and NE output without affecting the SNS- and muscarine- induced increases in EPI and NE output. From these results, it seems likely that the inhibition by cilnidipine of the SNS-induced EPI and NE secretion and of the muscarine-induced NE secretion is related to its blocking action on N-type VDCCs.
KW - Acetylcholine
KW - Adrenal catecholamine
KW - Cilnidipine
KW - L-type and N-type voltage-dependent Ca channels
KW - Nifedipine
KW - Splanchnic nerve stimulation
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U2 - 10.1097/00005344-199809000-00020
DO - 10.1097/00005344-199809000-00020
M3 - Article
C2 - 9733363
AN - SCOPUS:0031664129
VL - 32
SP - 479
EP - 484
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 3
ER -