作者: M B Taubman , B C Berk , B Nadal-Ginard , T Tsuda , S Izumo
DOI: 10.1016/S0021-9258(17)31290-5
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摘要: Abstract Vasoconstrictors such as angiotensin II (Ang II) play an important role in the pathogenesis of hypertension. These agonists may be responsible for abnormal vascular smooth muscle cell (VSMC) growth seen hypertension, either indirectly a consequence elevating blood pressure or directly result receptor-mediated effects on VSMC growth. To investigate whether Ang might initiate modulate some "early" genetic programs associated with VSMC, expression proto-oncogene c-fos was studied cultured rat aortic VSMC. rapidly induced accumulation mRNA, maximal levels occurring at approximately 30 min. Induction mRNA by concentration-dependent, response 100 nM. induction blocked its competitive inhibitor, [sarcosine 1,isoleucine 8]angiotensin II. not dependent upon II-stimulated intracellular alkalinization activation Na+/H+ exchange, but mobilization Ca2+ and protein kinase C activation. Epidermal factor, mitogen, also mechanism different from that results demonstrate vasoconstrictor hormone induces one earliest genes, c-fos, proliferative response.