Last month, we had come across a study that revealed a link between COPD and slow heart function. Experts from the Robarts Research Institute at The University of Western Ontario working in collaboration with scientists in Brazil seem to have spotted one more contributor to heart failure. Interestingly genetically modified mice appear to have revealed this earlier unidentified mechanism adding to heart failure.
Using the distinct genetically-modified mouse line, the investigators could recognize a previously unknown mechanism probably contributing to heart failure. The study demonstrated the effects of the decreased release of the neurotransmitter acetylcholine. Apparently lowered release of the chemical messenger seemed to slow cardiac activity allegedly contributing to heart failure.
The study was led by Marco Prado, Robert Gros and Vania Prado of London, Canada and Silvia Guatimosim of Brazil. With heart failure affecting close to a half million Canadians, often it is a result of conditions like coronary disease, high blood pressure, diabetes and high alcohol or drug consumption.
Two opposing divisions of the autonomic nervous system seem to be controlling cardiac output. It is known to be the sympathetic nervous system which could boost the heart rate and the parasympathetic system which may slow 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,” elucidated Gros, a cardiovascular researcher and assistant professor in the Departments of Physiology & Pharmacology and Medicine at Western’s Schulich School of Medicine & Dentistry.
“What we’re 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 added.
The line of mice was reportedly genetically modified by Marco and Vania Prado to include decreased secretion of acetylcholine. This was done originally for use in examining neuronal function in diseases like Alzheimer’s. However over time they discovered these mice developed alterations in their hearts which seemed to have progressively lowered their ability to pump blood. It was observed to be similar to what occurs with heart failure in humans.
“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,” shares Marco Prado, a professor in the Departments of Physiology & Pharmacology and Anatomy & Cell Biology. “One striking finding in this study is that heart dysfunction in these mice could be corrected by treating the animals with an existing drug which increases acetylcholine levels. Although it requires further study, this could provide a novel opportunity for treating failing hearts.”
Presently the drug, Pyridostigmine, is known to be approved for use in treating certain cases of muscle weakness.
This novel study is published online in Molecular and Cellular Biology.