TY - JOUR
T1 - Activation by α1-adrenergic Agonists of the progression phase in the proliferation of primary cultures of smooth muscle cells in mouse and rat aorta
AU - Mimura, Yasuhiko
AU - Horikoshi, Isamu
AU - Kobayashi, Shinjiro
AU - Notoya, Kouhei
AU - Okabe, Motonori
AU - Kimura, Ikuko
AU - Kimura, Masayasu
PY - 1995
Y1 - 1995
N2 - The effects of catecholamines on the competence and progression phases in the proliferation of vascular smooth muscle cells (SMCs) in mouse and rat were investigated in primary cultures. α,β-Adrenergic agonists such as epinephrine and norepinephrine, and the α-adrenergic agonist, phenylephrine, stimulated proliferation of primary cultured SMCs, whereas the α2-adrenergic agonist, clonidine, and β-adrenergic agonist, isoproterenol, did not. The stimulating effect of epinephrine was maximal at 0.54 μM and was then decreased at higher concentrations. The α-adrenergic antagonist, phentolamine, and α1-adrenergic antagonist, prazosin, inhibited epinephrine-induced SMC proliferation, while the α2-adrenergic antagonist, yohimbine, and β-adrenergic antagonist, propranolol, did not. In primary cultured and synchronized SMCs at the G0 phase, norepinephrine accelerated the rate of SMC proliferation, but did not change the starting time of DNA synthesis and proliferation. These results show that catecholamines activate the progression phase in primary cultured aortic SMCs α1-adrenergic receptors.
AB - The effects of catecholamines on the competence and progression phases in the proliferation of vascular smooth muscle cells (SMCs) in mouse and rat were investigated in primary cultures. α,β-Adrenergic agonists such as epinephrine and norepinephrine, and the α-adrenergic agonist, phenylephrine, stimulated proliferation of primary cultured SMCs, whereas the α2-adrenergic agonist, clonidine, and β-adrenergic agonist, isoproterenol, did not. The stimulating effect of epinephrine was maximal at 0.54 μM and was then decreased at higher concentrations. The α-adrenergic antagonist, phentolamine, and α1-adrenergic antagonist, prazosin, inhibited epinephrine-induced SMC proliferation, while the α2-adrenergic antagonist, yohimbine, and β-adrenergic antagonist, propranolol, did not. In primary cultured and synchronized SMCs at the G0 phase, norepinephrine accelerated the rate of SMC proliferation, but did not change the starting time of DNA synthesis and proliferation. These results show that catecholamines activate the progression phase in primary cultured aortic SMCs α1-adrenergic receptors.
KW - catecholamine
KW - cell proliferation
KW - primary culture
KW - progression phase
KW - smooth muscle cell
KW - α-adrenergic receptor
UR - http://www.scopus.com/inward/record.url?scp=0028787669&partnerID=8YFLogxK
U2 - 10.1248/bpb.18.1373
DO - 10.1248/bpb.18.1373
M3 - 学術論文
C2 - 8593439
AN - SCOPUS:0028787669
SN - 0918-6158
VL - 18
SP - 1373
EP - 1376
JO - Biological and Pharmaceutical Bulletin
JF - Biological and Pharmaceutical Bulletin
IS - 10
ER -