Table 2.

Main drugs and molecules which may have a role against IHD using ion channels as therapeutic target.

Drug	Biological effects	Functions
Sulphonylureas	Antagonist of the SUR subunit of pancreatic β-cell KATP	Promotion of β-cell depolarization and insulin secretion
Pinacidil and cromakalim	Kir6.2/SUR2A KATP and Kir6.2/SUR2B KATP channel openers	(i) Arteriole resistance reduction (ii) Arterial blood pressure reduction (iii) Vasodilatation
Nicorandil	Nitrate-like and proangiogenetic effect, calcium channel blocker, M2 macrophage polarization stimulator, M1 macrophage polarization inhibitor, and NF-κB p65 subunit inhibitor	(i) Prevention of ventricular arrhythmias in patients who underwent coronary angioplasty after acute myocardial infarction (ii) Reduction of macrophage phagocytic activity, ROS and cytokine production, and improvement of mitochondrial membrane stability and Bcl-2/Bax ratio (iii) Promotion of endothelial reconstitution (iv) Improvement of the prognosis of patients with stable angina
Levosimendan	mBKCa-channel activator and calcium sensitizer, KATP activator	(i) Heart pump function improvement and reduction of the risk to develop arrhythmic events after myocardial ischemia (ii) Vasodilatation and increase in CBF
Isosteviol sodium	ROS scavenger	(i) Inhibition of QTc prolongation related to ischemia/reperfusion injury and reduction of Ikr and Ikatp channel inhibition during ischemia/reperfusion injury
N-3-PUFA	Coronary BKCa channel activation, Ca2+ concentration in coronary smooth muscle cell reduction	(i) Vasodilation and increase in CBF
NOX inhibitor	ROS reduction
Nrf-2 activator	Catalase and erythrocyte SOD activity induction in vivo
Vitamin E	Antioxidant activity