Abstract:
:In order to elucidate the signal transduction pathway of vascular smooth muscle contraction induced by the activation of receptors for angiotensin II and endothelin-1, we examined whether tyrosine kinases and mitogen-activated protein (MAP) kinases are involved in the development of force of contraction in the rat aorta. Isolated aortic smooth muscles without endothelium were incubated in a modified Krebs-Henseleit solution and stimulated with angiotensin II (100 nM) or endothelin-1 (10 nM). A tyrosine kinase inhibitor genistein (10 microM) reduced the angiotensin II- and endothelin-1-induced aortic contraction, while 10 microM of daidzein (an inactive analogue of genistein) did not. The K(+) depolarization-induced contraction was not attenuated by 10 microM of genistein. Selective inhibitors of MAP kinase/extracellular signal-regulated kinase (Erk) kinase (MEK) such as PD98059 [2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one] and U0126 [1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene] inhibited the angiotensin II- and endothelin-1-induced vasocontraction. The p44/42 MAP kinases were phosphorylated in cultured aortic smooth muscle cells and in physiologically contracted aortic vessels stimulated with angiotensin II and endothelin-1 for 5 min. The angiotensin II- and endothelin-1-induced phosphorylations of p44/42 MAP kinases were inhibited by PD98059 as well as U0126 in the intact aorta. These results suggest that the activation of genistein-sensitive tyrosine kinases and p44/42 MAP kinases is involved in the angiotensin II- and endothelin-1-induced rat aortic contraction.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Ishihata A,Tasaki K,Katano Ydoi
10.1016/s0014-2999(02)01790-9keywords:
subject
Has Abstractpub_date
2002-06-12 00:00:00pages
247-56issue
3eissn
0014-2999issn
1879-0712pii
S0014299902017909journal_volume
445pub_type
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