【Objective】 To compare the differences between the effects of protein kinase C (PKC) and protein tyrosine phosph-orylation on volume-regulated chloride channel (VRCC) during the phenotype modulation of smooth muscle cells in artery and vein. 【Methods】 We used the whole cell patch clamp to evaluate swelling induced Cl- currents (ICl

vol) in primay

Ⅳ and Ⅷ passage rat femoral artery (FASMC) and vein smooth muscle cells (FVSMC); and the regulative the effects of protein tyrosine kinase (PTK) inhibitor genistein

protein tyrosine phosphatase (PTP) inhibitor sodium orthovanadate

and PKC activator PDBu on VRCC activity in these cells were examined. 【Results】 Hypotonic solution induced larger ICl

vol in FASMC than in FVSMC. PTK inhibitor genistein and PKC activator PDBu inhibited VRCC activity in both FASMC and FVSMC

and this inhibitory effect was gradually enhanced in the cells from primary to passage Ⅷ. Whereas PTP inhibitor sodium orthovanadate increased VRCC activity in both FASMC and FVSMC

and this increase was gradually decreased as cell passages increased. Moreover

at the same cell passage

the regulatory effects of genistein

PDBu

and sodium orthovanadate on VRCC activity were more prominent in FVSMC than in FASMC. 【Conclusion】 PTK

PTP

and PKC could regulate VRCC activity

which were more prominent in FVSMC than in FASMC. Moreover

VRCC activity and the regulatory effects of PKC and protein tyrosine phosphorylation on VRCC were gradually increased as vascular cells switch from contractile to proliferative phenotypes.