Toronto: Canadian and Brazilian scientists have revealed an unknown mechanism that contributes to heart failure.
In their joint study, the scientists have found that the decreased release of the neurotransmitter acetylcholine - a chemical messenger which slows cardiac activity - contributes to heart failure.
The researchers - Marco Prado, Robert Gros and Vania Prado from the University of Western Ontario in Canada and Silvia Guatimosim of Brazil - used a unique genetically-modified mice to reveal this previously unidentified mechanism contributing to heart failure, a statement by the University of Western Ontario says.
Heart failure results from a combination of conditions, including coronary disease, high blood pressure, diabetes and high alcohol or drug consumption.
The scientists say cardiac activity is controlled by two opposing divisions of the autonomic nervous system - the sympathetic nervous system which boosts the heart rate and the parasympathetic system which slows it by releasing acetylcholine.
"Lots of people have studied the system that increases the heart rate and that has been the hallmark; we know there`s an increase in the sympathetic nervous system in people who have heart failure," says Robert Gros, who is a cardiovascular researcher at the Canadian university, in the statement.
"What we are now showing with this mouse model is that even if you have a functional sympathetic nervous system, if the other system, the parasympathetic system is dysfunctional or works less optimally than normal, you still end up with a sick heart. This opens up a whole new avenue that people have missed in the past," he says.
Actually, these researchers had genetically modified a line of mice with decreased secretion of acetylcholine to study neuronal function in diseases such as Alzheimer`s. But they found that these mice, over time, developed changes in their hearts that decreased their ability to pump blood, similar to what occurs with heart failure in humans, the statement said.
"There are other mouse and rat models of heart failure, but what we haven`t had before is a model where we specifically target this chemical messenger, acetylcholine," researcher Marco Prado has been quoted as saying.
"One striking finding in this study is that heart dysfunction in these mice could be corrected by treating the animals with an existing drug (Pyridostigmine) which increases acetylcholine levels. Although it requires further study, this could provide a novel opportunity for treating failing hearts," the Canadian said.
The study has been published online in Molecular and Cellular Biology.