Myocardial Infarction
Afterload-induced exacerbation of infarct size is linked to T-type Ca2+ channel activity
Published in Cardiovascular Week, June 12th, 2006
According to recent research published in the journal Hypertension, "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,"...
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Source: Cardiovascular Week (2006-06-12)
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