Endothelin-1 induces intracellular [Ca2+] increase via Ca 2+ influx through the L-type Ca2+ channel, Ca 2+ -induced Ca2+ release and a pathway involving ET A receptors, PKC, PKA and AT1 receptors in cardiomyocytes.

Using fura-2-acetoxymethyl ester (AM) fluorescence imaging and patch clamp techniques, we found that endothelin-1 (ET-1) significantly elevated the intracellular calcium level ([Ca(2+)](i)) in a dose-dependent manner and activated the L-type Ca(2+) channel in cardiomyocytes isolated from rats. The effect of ET-1 on [Ca(2+)](i) elevation was abolished in the presence of the ET(A) receptor blocker BQ123, but was not affected by the ET(B) receptor blocker BQ788. ET-1-induced an increase in [Ca(2+)](i), which was inhibited 46.

[Current alteration of K(V) channel in SLE patient's peripheral blood lymphocytes and it's significant].

Aim: To observe the property alteration of K(v) channel in SLE patient's peripheral blood lymphocyte and its significant.

Methods: The patch-clamp technique was used to record the current of K(V) channel in SLE patient's peripheral lymphocyte.

Results: The current amplitude of K(V) channel in the SLE patient's lymphocytes decreased, it was (258.