Protective effect of some calcium antagonists against mitochondrial calcium injury.
Ischaemia induces an increase in calcium cytosolic concentration, leading to a mitochondrial Ca2+ overload. As Ca2+ uptake and storage into mitochondria are the alternative route to oxidative phosphorylation, the Ca2+ overload induces a decrease in ATP synthesis. We have tested in vitro the ability of certain calcium antagonists to restore the ATP synthesis inhibited by mitochondrial calcium overload. Our results showed that diltiazem and bepridil, clinically used as antiischaemic agents, each can restore the ATP synthesis. It is suggested that our in-vitro results might serve to explain the antiischaemic properties of some calcium antagonists.
Tabouy
L
L
Chauvet-Monges
A M
AM
Salducci
M D
MD
Crevat
A
A
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D017311:Amlodipine / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D015764:Bepridil / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004110:Diltiazem / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000188:drug therapy; D009529:Nicardipine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014700:Verapamil / Q000494:pharmacology
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D017311:Amlodipine; D015764:Bepridil; D000255:Adenosine Triphosphate; D014700:Verapamil; D009529:Nicardipine; D004110:Diltiazem