|Budget Amount *help
¥3,000,000 (Direct Cost : ¥3,000,000)
Fiscal Year 1998 : ¥1,300,000 (Direct Cost : ¥1,300,000)
Fiscal Year 1997 : ¥1,700,000 (Direct Cost : ¥1,700,000)
Restenosis after an initial successful percutaneous transluminal coronary angioplasty (PTCA) remains a signifiant clinical problem. The mechanisms that underlie restenosis are still unclear. Initial reports have documented a proliferative cellular response as the main pathological feature. More recently, so-called late remodeling has been introduced as a mechanism, although the processes causing this phenonenon are unclear still.
The present study demonstrates that, during neointimal formation at the site of PTCA, smooth muscle cells show phenotypic changes, indicated by altered expression of smooth muscle myosin heavy chain (Circulation 96 : 82-90, 1997). The present study, moreover, documents that up-regulation of angiotensin converting enzyme and endothelin converting enzyme occurs during neointimal formation after PTCA, especially at the early stage of neointimal formation. (Circulation 96 : 3328-3337, 1997 ; J.Hypertens, 15 : 1295-1302 ; Circulation 96 : I-348, 1997). Furthermore, The present study reveals that the expression of endothelin type A receptor is also up-regulated in neointimal smooth muscle cells at the site of PTCA (Circularion 98 : I-734, 1998)