TY - JOUR
T1 - Muscarinic acetylcholine receptor-mediated increase of angiotensin type 2 receptor mRNA in PC12 cells
AU - Shibata, Kazuhiko
AU - Ikuko, Makino
AU - Inoue, Kazuhide
AU - Katsuragi, Takeshi
PY - 1998/12/1
Y1 - 1998/12/1
N2 - The present study examined changes in the angiotensin type 2 (AT2) receptor mRNA level after carbachol exposure in PC12 cells. The AT2 receptor mRNA level increased 2- to 3-fold after 12-18 h of carbachol exposure (100 μM). The up-regulation of AT2 receptor mRNA was antagonized by atropine, which is a muscarinic receptor antagonist, thus suggesting that the increase in AT2 receptor mRNA is mediated via muscarinic acetylcholine receptors. This increase is blocked by N(G)-nitro-L-arginine-methylester, nitric oxide (NO) synthase inhibitor, and hemoglobin NO trap. Protein kinase C (PKC) inhibitors, H-7 and calphostin C, inhibited the carbachol-induced upregulation. In addition, a G kinase inhibitor, ODQ (1H- [1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one), inhibited this increase. These findings suggest that the carbachol-induced increases in AT2 receptor mRNA is regulated by the activation of NO-cGMP and/or the PKC pathway.
AB - The present study examined changes in the angiotensin type 2 (AT2) receptor mRNA level after carbachol exposure in PC12 cells. The AT2 receptor mRNA level increased 2- to 3-fold after 12-18 h of carbachol exposure (100 μM). The up-regulation of AT2 receptor mRNA was antagonized by atropine, which is a muscarinic receptor antagonist, thus suggesting that the increase in AT2 receptor mRNA is mediated via muscarinic acetylcholine receptors. This increase is blocked by N(G)-nitro-L-arginine-methylester, nitric oxide (NO) synthase inhibitor, and hemoglobin NO trap. Protein kinase C (PKC) inhibitors, H-7 and calphostin C, inhibited the carbachol-induced upregulation. In addition, a G kinase inhibitor, ODQ (1H- [1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one), inhibited this increase. These findings suggest that the carbachol-induced increases in AT2 receptor mRNA is regulated by the activation of NO-cGMP and/or the PKC pathway.
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M3 - Article
C2 - 9875705
AN - SCOPUS:0032424242
SN - 0959-4965
VL - 9
SP - 3783
EP - 3789
JO - NeuroReport
JF - NeuroReport
IS - 17
ER -