MEDIATORS OF PERIVASCULAR INFLAMMATION IN THE LEFT-VENTRICLE OF RENOVASCULAR HYPERTENSIVE RATS

Objective: Inflammatory cells invade the fibrotic myocardium of sponta neously hypertensive rats at the same sites as where fibroblasts are p roduced. The role of these inflammatory cells in myocardial fibrogenes is was studied in the present work. Methods: The production and distri bution of proteins that may be implicated in inflammation was examined by immunohistochemistry of sections of left ventricles from 1-month a nd 4-month renovascular hypertensive and age-matched control rats usin g antibodies against ICAM-1, LFA-1, TGF beta 1, PDGF-A, T and H kinino gens, IgG, IgM, C3, and C5b-9. Infiltrating inflammatory cells were ph enotyped by immunohistochemistry. The TGF beta 1 and PDGF-A mRNA level s were checked by RT-PCR. Results: Infiltrating cells were mainly T he lper lymphocytes and macrophages, and there were more inflammatory cel ls in hypertensive rats than in control rats, localized especially aro und coronary arteries and in microscars. There were more ICAM-1 and LF A-1 in the ventricles of hypertensive than in control rats at 1 month, but the ICAM-1 expressions in hypertensive and control rats were simi lar at 4 months. TGF beta 1 and PDGF-A mRNA steady states increased in 4-month hypertensive rats, but there was no labeling for TGF beta or PDGF by immunohistochemistry. There was only faint labeling for T and H kininogens, and it was not increased in hypertensive rats. There wer e deposits of IgM and C5b-9 only in hypertensive rats, Conclusion: Thu s, inflammatory cells infiltrate the cardiac tissue of renovascular hy pertensive rats as in the case of spontaneously hypertensive rats and these cells may use the ICAM-1/LFA-1 system to infiltrate, but neither TGF beta 1 and PDGF-A, nor the kininogen system seem to be associated with cardiac fibrogenesis. Otherwise, the complement system could act as arteriosclerotic and/or leukocyte mobilizing factors.