ABSTRACT
AIM To investigate the pathways of Ca 2+ entry into ECV304 endothelial cell and the effect of angiotensin Ⅱ(AⅡ) on calcium activated non setective cation channel(CAN). METHODS The cell attachment and whole cell configurations of patch clamp technique were used to record channel activity. RESULTS (1) The single channel conductance is ? o=(12 90?2 11) pS( n =4) for Ca 2+ passing through CAN of ECV304 cell in condition of pipette solution without K + and Na + but composed 120 mmol?L -1 CaCl 2. The channel current amplitude and open time can be enhanced by 1?10 -7 mol?L -1 AⅡ. The enhanced conductance in CAN is ? 1=(22 18?2 29) pS( n =4). The results of whole cell recording are identified with single channel recording. (2) The whole cell configuration was carried out for recording voltage dependent Ca 2+ channel in ECV304 cell. The peak current amplitude was (29 32?3 56) pA( n =4). This current was inhibited to (6 00?3 94) pA( n =4) by nifedipine and activated by BayK8644. CONCLUSIONS (1)Ca 2+ enters ECV304 cell via Ca 2+ activated non selective cation channel and voltage dependent L type calcium channel. (2) AⅡ can significantly enhance the calcium entry via CAN in ECV304 cell.
ABSTRACT
The H2O2 has been shown to have comprahensive actions on various ion channels of cell membrane. But it has different effects on different tissues. H2O2-induced a dose dependent decreasing L- type Ca2+ current on cultrued Lymnaea neurons. In sheep cardiac SR, H2O2 plays an important role in regulating directly on RyR Ca2+-release channel that caused an increasing of P0, but it was no effects on conductance. It indicated that H2O2-induced different activities on KCa channel with different tissues. In guinea pig ventricular myocytes, H2O2-induced increase in KATP channels. There are few data on the effects of H2O2 on whole cell Na+ currents and single Na+ channels.