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CA2 — INA
Text-mined interactions from Literome
Boccara et al., Circ Res 1999
:
In conclusion,
I(Na) regulates [
Ca2+ ] i in primary cultured HCMs
Jans et al., Pflugers Arch 2000
(Ion Channel Gating) :
At constant osmolality ( 200 mOsm/kg H2O ) 10 mM Mg2+ increased I(Na), leaving C ( T ) unaffected, whereas 10 mM
Ca2+ stimulated both
I(Na) and CT
Lipp et al., J Physiol 2002
(Calcium Signaling) :
In contrast,
I(Na) induced
Ca2+ responses were still spatially homogeneous and lacked Ca2+ sparks even for small current amplitudes
Fraser et al., J Mol Cell Cardiol 2006
(Myocardial Ischemia...) :
Augmentation of late
INa with sea anemone toxin-II ( ATX-II, 12 nM ) increased diastolic [Ca2+ ] i ( d [ Ca2+ ] i ), and impaired LV mechanical function, but
had no effect on
[Ca2+ ] i transient amplitude
Levesque et al., Ann N Y Acad Sci 1991
:
This result provides direct evidence that Ca2+ entry via reverse-mode Na(+)-Ca2+ exchange mediates the
INa induced SR
Ca2+ release ... The
INa induced release of
Ca2+ from SR may partially account for the positive inotropic effects of cardiac glycosides and the negative inotropic effects of antiarrhythmic drugs that block Na+ channels
Krattenmacher et al., J Comp Physiol B 1990
:
Removal of
Ca2+ from the mucosal Ringer solution
stimulated INa by about 120 %
Lipp et al., J Physiol 1994
:
Analysis of
INa induced
Ca2+ signals at higher temporal resolution revealed a faster upstroke of these transients when compared with those triggered by ICa ...
INa also
induced a residual
Ca2+ transient that was insensitive to 10 microM verapamil and characterized by a rapid upstroke ... This result supports the notion that both the residual Ca2+ transient as well as the
INa induced
Ca2+ release are mediated by the Na(+)-Ca2+ exchange. ( ABSTRACT TRUNCATED AT 250 WORDS )
Cox et al., J Vasc Res 1998
(Ion Channel Gating) :
Lowering external
[Ca2+ ] to zero
increased the maximum
INa , shifted its voltage dependence in the hyperpolarizing direction and increased the rate of INa inactivation