Mechanisms underlying afterload-induced exacerbation of myocardial infarct size: role of T-type Ca2+ channel

Hypertension
Mahmood S MozaffariStephen W Schaffer

Abstract

One consequence of elevated afterload pressure is the activation of the angiotensin II type 1 receptor and nonspecific cation channels with subsequent Ca2+ accumulation via the Na+/H(+)-Na+/Ca2+ exchanger combination and the T-type or L-type Ca2+ channels. Intracellular Ca2+ overload is cytotoxic, in part, by inducing the mitochondrial permeability transition (MPT) pore. Therefore, we tested the hypotheses that: (1) increased afterload pressure worsens myocardial ischemia-reperfusion injury in healthy heart, (2) the Na+/H(+)-Na+/Ca2+ exchanger combination and both the T-type and L-type Ca2+ channels are involved in the exacerbating impact of high afterload pressure on infarct size, and (3) elevated afterload enhances infarct size in part via the MPT pore. Accordingly, the effect of candesartan (angiotensin II type 1 receptor antagonist), cariporide (inhibitor of the Na+/H+ exchanger), mibefradil (T-type Ca2+ channel blocker), diltiazem (L-type Ca2+ channel blocker), or cyclosporine A (inhibitor of MPT pore) were examined. The elevation in afterload pressure from 80 to 160 cmH2O increased baseline myocardial performance but caused larger infarcts and worsened recovery of mechanical function after ischemia reperfusion. Whereas mi...Continue Reading

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Citations

Aug 23, 2008·Obesity·Mahmood S Mozaffari, Stephen W Schaffer
Apr 26, 2008·American Journal of Hypertension·Mahmood S Mozaffari, Stephen W Schaffer
Mar 20, 2010·American Journal of Hypertension·Mahmood S MozaffariStephen W Schaffer
Jun 1, 2019·Pharmacology Research & Perspectives·Olivia J Robertson-GrayCherry L Wainwright
Nov 22, 2015·Journal of Cardiovascular Pharmacology and Therapeutics·Chris PantsiosKonstantinos Malliaras

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