depolarized

SR33805 是钙通道拮抗剂，在去极化和极化条件下的 EC50值分别为 4.1 和 33 nM。它阻止 L 型 Ca2+通道，可用于研究急性或慢性心脏衰竭。

Bisaramil hydrochloride (Bisaramil) 是一种新型二氮双环壬烷抗心律失常化合物，抑制自由基生成。Bisaramil hydrochloride 可阻断钠电流，抑制异丙肾上腺素在 K（+） 去极化肌上诱导的缓慢 Ca（2+） 动作电位。

F 15845 is a blocker of the persistent sodium current prevents consequences of hypoxia in rat femoral artery. F15845 has been shown to selectively inhibit the persistent sodium current of Nav1.5[1] exerting cardioprotective effects following ischemia. In vitro testing showed minimal effects of F15845 on other important ion channels of the heart, including major Ca2+ and K+ channels.[1] This characteristic is thought to account for the limited effect of F15845 to change other heart parameters such as basal cardiac function, hemodynamic functions and ventricular fibrillation. F15845 was also shown to exert improved effects when the membrane potential was depolarized,[1] by acting on the extracellular side of the channel.

Nicorandil-d4 is intended for use as an internal standard for the quantification of nicorandil by GC- or LC-MS. Nicorandil is an activator of sulfonylurea receptor 2B (SUR2B) linked to ATP-sensitive potassium channel Kir6.2 (EC50 = ~10 µM) and a nitric oxide (NO) donor. It is selective for SUR2B Kir6.2 over the SUR2A Kir6.2 channel (EC50 = >500 µM). Nicorandil activates soluble guanylate cyclase in a cell-free assay and relaxes partially depolarized isolated bovine coronary artery strips (EC50 = 4.4 µM). It decreases mean blood pressure, coronary resistance, and heart rate, as well as increases coronary sinus outflow, in dogs when administered intravenously at a dose of 1 mg kg. Nicorandil increases survival and decreases infarct size in a rabbit model of myocardial ischemia-reperfusion injury induced by left coronary artery occlusion. Formulations containing nicorandil have been used in the treatment of angina pectoris.

Guangxitoxin 1E acts as a gating modifier since it shifts the voltage-dependence of Kv2.1 K+ currents towards depolarized potentials.