Ionic mechanisms of a novel neurotoxin from the sea anemone Anthopleura sp. in rat ventricular myocytes.
OBJECTIVE
To determine the ionic mechanisms of a novel neurotoxin rhk2a obtained from the sea anemone Anthopleura sp. in rat ventricular myocytes.


METHODS
Whole-cell patch-clamp recording technique was used to record the sodium, calcium, and sodium-calcium exchange currents (I(Na), I(Ca, L), and I(Na-Ca), respectively) in the isolated single rat ventricular myocytes with or without rhk2a treatment.


RESULTS
The current-voltage (I-V) relationship for whole-cell I(Na) in the non-treated and rhk2a-treated (at the dose of 1 micromol/L) myocytes showed no significant difference (P>0.05), but the time constants for inactivation (tau(h)) were significantly greater (P<0.05) for the treated cells over the entire course of the experiment, while the time constants for activation (tau(m)) exhibited no significant difference between the two cells. The inactivation curve of I(Na) of rhk2a-treated cells was similar to that of the non-treated cells, as with the I-V relationship for whole-cell L-type calcium current (I(Ca, L) and I(Na-Ca)).


CONCLUSIONS
Delayed inactivation of Na(+) channel plays an important role in the positive inotropic effect of rhk2a, possibly resulting from the alteration in Na(+) channel kinetics induced by rhk2a. rhk2a does not directly affect I(Ca, L), or I(Na-Ca).
Ouyang
Ping
P
Department of Cardiology, Nanfang Hospital, First Military Medical University, Guangzhou, 510515, China.
Deng
Chun-yu
CY
Liu
Wen-hua
WH
Wang
Lei
L
Liang
Dong
D
Qian
Wei-min
WM
Xu
An-long
AL
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects* / Q000502:physiology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D003064:Cnidarian Venoms / Q000494:pharmacology*; D006352:Heart Ventricles; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000502:physiology; D009498:Neurotoxins / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000494:pharmacology; D015222:Sodium Channels / Q000187:drug effects* / Q000502:physiology
D015220:Calcium Channels; D002316:Cardiotonic Agents; D003064:Cnidarian Venoms; D009498:Neurotoxins; D011994:Recombinant Proteins; D015222:Sodium Channels