Abstract:
:The present experiments were devoted to analyzing the mechanisms involved in the captopril-dependent inhibition of human mesangial cell proliferation. Studies were performed in cultured human mesangial cells incubated with captopril, an angiotensin II-converting enzyme inhibitor with antioxidant properties, lisinopril, a non-antioxidant angiotensin II-converting enzyme inhibitor, and tocopherol, a pure antioxidant. Both angiotensin II-converting enzyme inhibitors significantly inhibited fetal calf serum-induced [3H]thymidine uptake by human mesangial cells, in a dose- and time-dependent manner, an effect which was not observed with tocopherol. The antiproliferative effect of captopril and its ability to block tyrosine phosphorylation of human mesangial cells proteins were significantly greater than those of lisinopril. Moreover, captopril significantly prevented the fetal calf serum-induced tyrosine phosphorylation of pp60(c-src). The present results suggest that the antiproliferative ability of captopril does not completely depend on its angiotensin II-converting enzyme inhibitor properties, pointing to a possible interaction of the drug with the intracellular mechanisms responsible for the transmission of the proliferative signals.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Ruiz-Ginés JA,Pérez-Caballero C,O'Valle F,Rodríguez-Puyol M,Rodríguez-Puyol Ddoi
10.1016/s0014-2999(97)01250-8subject
Has Abstractpub_date
1997-10-08 00:00:00pages
251-6issue
2-3eissn
0014-2999issn
1879-0712pii
S0014-2999(97)01250-8journal_volume
336pub_type
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