Sydney Ringer would be overwhelmed today by the implications of his
simple experiment performed over 120 years ago showing that the heart
would not beat in the absence of Ca$^2+$. Fascination with the
role of Ca$^2+$ has proliferated into all aspects of our understanding
of normal cardiac function and the progression of heart disease,
including induction of cardiac hypertrophy, heart failure, and sudden
death. This review examines the role of Ca$^2+$ and the L-type
voltage-dependent Ca$^2+$ channels in cardiac disease.
%0 Journal Article
%1 Bodi_2005_3306
%A Bodi, Ilona
%A Mikala, Gabor
%A Koch, Sheryl E
%A Akhter, Shahab A
%A Schwartz, Arnold
%D 2005
%J J. Clin. Invest.
%K 16322774 Acid Amino Animals, Atrial Biological, Calcium Calcium, Calmodulin, Cardiac, Channels, Congestive, Distribution, Extramural, Failure, Fibrillation, Heart Humans, Isoforms, L-Type, Models, Motifs, Myocytes, N.I.H., Protein Research Structure, Support, Tertiary, Tissue
%N 12
%P 3306--3317
%R 10.1172/JCI27167
%T The L-type calcium channel in the heart: the beat goes on.
%U http://dx.doi.org/10.1172/JCI27167
%V 115
%X Sydney Ringer would be overwhelmed today by the implications of his
simple experiment performed over 120 years ago showing that the heart
would not beat in the absence of Ca$^2+$. Fascination with the
role of Ca$^2+$ has proliferated into all aspects of our understanding
of normal cardiac function and the progression of heart disease,
including induction of cardiac hypertrophy, heart failure, and sudden
death. This review examines the role of Ca$^2+$ and the L-type
voltage-dependent Ca$^2+$ channels in cardiac disease.
@article{Bodi_2005_3306,
abstract = {Sydney Ringer would be overwhelmed today by the implications of his
simple experiment performed over 120 years ago showing that the heart
would not beat in the absence of {C}a$^{2+}$. Fascination with the
role of {C}a$^{2+}$ has proliferated into all aspects of our understanding
of normal cardiac function and the progression of heart disease,
including induction of cardiac hypertrophy, heart failure, and sudden
death. This review examines the role of {C}a$^{2+}$ and the L-type
voltage-dependent {C}a$^{2+}$ channels in cardiac disease.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Bodi, Ilona and Mikala, Gabor and Koch, Sheryl E and Akhter, Shahab A and Schwartz, Arnold},
biburl = {https://www.bibsonomy.org/bibtex/24be2e9fd2f023760d38620568cccc47f/hake},
description = {The whole bibliography file I use.},
doi = {10.1172/JCI27167},
interhash = {044c7344d970227b6dce6778339cf11c},
intrahash = {4be2e9fd2f023760d38620568cccc47f},
journal = {J. Clin. Invest.},
keywords = {16322774 Acid Amino Animals, Atrial Biological, Calcium Calcium, Calmodulin, Cardiac, Channels, Congestive, Distribution, Extramural, Failure, Fibrillation, Heart Humans, Isoforms, L-Type, Models, Motifs, Myocytes, N.I.H., Protein Research Structure, Support, Tertiary, Tissue},
month = Dec,
number = 12,
pages = {3306--3317},
pmid = {16322774},
timestamp = {2009-06-03T11:21:06.000+0200},
title = {The L-type calcium channel in the heart: the beat goes on.},
url = {http://dx.doi.org/10.1172/JCI27167},
volume = 115,
year = 2005
}