csa induced chronic ischemia begins with arteriolar vasoconstriction and subsequently proceeds with the hyalinosis. intra--renal renin angiotensin system activation is an important mechanisms for csa induced vasoconstriction [4,7,8,11,12,34--40]. carvedilol is a potent vasodilator agent which blocks α1, β1, β2 adrenergic receptors and has antioxidant and anti--fibrotic effects. in a recent study, in vitro positive impacts of carvedilol on chronic nephrotoxicity have been shown [2,18,21,41]. we hypothesised that carvedilol might inhibit csa--induced sympathetic activity and might suppress renin angiotensin system activity via β receptors. our findings supported our hypothesis; carvedilol group alleviated biochemical and histopathological findings associated with csa usage. it reduces the activity of angiotensin ii, thereby renal blood flow and glomerular filtration rate are maintained [42,43]. however, the presence of apoptosis has been mainly recognized as a marker of chronic csa nephrotoxicity in which studies with similar modeling [30,44]. as apoptosis is the precursor lesion, if the study had continued, it was likely to be followed by other histopathological findings, especially fibrosis.