Abstract
ABSTRACTSpider venoms are known to contain various toxins that are used as an effective means to capture their prey or to defend themselves against predators. An investigation of the properties of Ornithoctonus huwena (O.huwena) crude venom found that the venom can block neuromuscular transmission of isolated mouse phrenic nerve-diaphragm and sciatic nerve-sartorius preparations. However, little is known about its electrophysiological effects on cardiac myocytes. In this study, electrophysiological activities of ventricular myocytes were detected by 100 μg/mL venom of O.huwena, and whole cell patch-clamp technique was used to study the acute effects of the venom on action potential (AP), sodium current (INa), potassium currents (IKr, IKs, Ito1 and IK1) and L-type calcium current (ICaL). The results indicated that the venom prolongs APD90 in a frequency-dependent manner in isolated neonatal rat ventricular myocytes. 100 μg/mL venom inhibited 72.3 ± 3.6% INa current, 58.3 ± 4.2% summit current and 54 ± 6.1% the end current of IKr, and 65 ± 3.3% ICaL current, yet, didn't have obvious effect on IKs, Ito1 and IK1 currents. In conclusion, the O.huwena venom represented a multifaceted pharmacological profile. It contains abundant of cardiac channel antagonists and might be valuable tools for investigation of both channels and anti- arrhythmic therapy development.
Highlights
The mammalian heart is a mechanical pump with the function of assuring pulmonary and systemic blood circulation
The venom prolongs APD in isolated neonatal rat ventricular myocytes To test the effect of the venom on action potential duration (APD) in isolated neonatal rat ventricular myocytes, APDs before and after the treatment of 100 mg/mL venom were determined (Figure 1)
Six prominent voltage-gated ion currents expressed in cardiac ventricular muscle are sodium current (INa), rapid activating delayed rectifier outward K+ current (IKr), slowly activating delayed rectifier outward K+ current (IKs), transient outward K+ current (Ito1), inward rectifier K+ current (IK1) and L-type calcium current (ICaL) [24]
Summary
The mammalian heart is a mechanical pump with the function of assuring pulmonary and systemic blood circulation. The outward currents are carried by four prominent K+ channels, containing the transient outward K+ current Ito, the rapidly and slowly activating delayed rectifier K+ currents (IKr and IKs) and the inward rectifier K+ current IK1, in cardiac ventricular myocytes. These K+ currents contribute to repolarization of different phases of the action potential [1,2,3,4]. The plateau phase depends on a delicate balance of inward (depolarizing) and outward (repolarizing) currents, and the depolarizing force is mainly a Ca2+ influx which slowly declines as L-type calcium channels inactivate, and non-inactivating Na+ current can support the plateau phase [5]. The repolarizing action depends on K+ efflux due to activation of several voltage-gated potassium channels
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