Up‐Regulation of Myocardial L‐Type Ca²⁺ Channel in Chronic Alcoholic Subjects Without Cardiomyopathy

Abstract

Chronic alcoholism causes an up-regulation of myocardial L-type Ca(2+) channel receptors, which decreases when cardiomyopathy is present.

The effect of an NO donor, pentaerythrityl tetranitrate, on biochemical, functional, and morphological attributes of cardiovascular system of spontaneously hypertensive rats

“…A similar situation was found in aorta, where endothelial NOS, CuZnSOD, MnSOD, and GPx, but not catalase (CAT) levels and activities were increased (Ulker et al 2003;Racasan et al 2005). In humans, superoxide dismutase activity was related to the presence of cardiac enlargement and the degree of cardiac histological damage (Fatjó et al 2005).…”

Alcohol abuse and heart failure

“…Excitation–contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. L‐type Ca 2+ channels, involved in excitation–contraction coupling, are disturbed in animal models of persistent ethanol consumption . A report from Aistrup expands our understanding of the changes in cellular excitation–contraction coupling in cardiac myocytes during the transition period where acute ethanol exposure becomes chronic.…”

“…L-type Ca 2þ channels, involved in excitation-contraction coupling, are disturbed in animal models of persistent ethanol consumption. 61 A report from Aistrup 62 expands our understanding of the changes in cellular excitation-contraction coupling in cardiac myocytes during the transition period where acute ethanol exposure becomes chronic. After the onset of chronic ethanol consumption, the welldocumented negative inotropic effect of acute ethanol exposure is temporarily counteracted by adaptive mechanisms, leading to the expression of a temporary positive inotropic effect.…”

Quercetin Attenuates Ethanol‐Induced Iron Uptake and Myocardial Injury by Regulating the Angiotensin II‐L‐Type Calcium Channel

“…Furthermore, long‐term alcohol exposure in rats resulted in increased activity of protein kinase C, which may be associated with changes in the regulation of cardiac LTCC . Moreover, in human samples, researchers found that chronic alcoholism results in upregulation of myocardial LTCC . In this study, we identified LTCC as the major transporter required for iron entry into cardiomyocytes in the alcohol‐induced myocardial iron‐overload model.…”