AI Article Synopsis

  • The compound N-arachidonoyl-L-serine (ARA-S) activates the Kv7.1/KCNE1 ion channel, which plays a crucial role in heart function, by shortening action potential duration and QT interval in guinea pig hearts.
  • A study using the two-electrode voltage clamp technique shows that ARA-S affects Kv7.1/KCNE1 channels similarly across guinea pig, rabbit, and human models, indicating broad applicability for research.
  • Findings suggest that both rabbit and guinea pig animal models are appropriate for further investigations of ARA-S's cardiac effects, given their comparable responses to the compound.

Article Abstract

The endogenous endocannabinoid-like compound N-arachidonoyl-L-serine (ARA-S) facilitates activation of the human Kv7.1/KCNE1 channel and shortens a prolonged action potential duration and QT interval in guinea pig hearts. Hence, ARA-S is interesting to study further in cardiac models to explore the functional impact of such Kv7.1/KCNE1-mediated effects. To guide which animal models would be suitable for assessing ARA-S effects, and to aid interpretation of findings in different experimental models, it is useful to know whether Kv7.1/KCNE1 channels from relevant species respond similarly to ARA-S. To this end, we used the two-electrode voltage clamp technique to compare the effects of ARA-S on Kv7.1/KCNE1 channels from guinea pig, rabbit, and human Kv7.1/KCNE1, when expressed in oocytes. We found that the activation of Kv7.1/KCNE1 channels from all tested species was facilitated by ARA-S, seen as a concentration-dependent shift in the voltage-dependence of channel opening and increase in current amplitude and conductance over a broad voltage range. The rabbit channel displayed quantitatively similar effects as the human channel, whereas the guinea pig channel responded with more prominent increase in current amplitude and maximal conductance. This study suggests that rabbit and guinea pig models are both suitable for studying ARA-S effects mediated via Kv7.1/KCNE1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520554PMC
http://dx.doi.org/10.1080/19336950.2024.2420651DOI Listing

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