Heart Cells Communicate to Regulate Organ Function

A recent study shows how heart cells communicate in order to better regulate heart activity.

Researchers from Western University (London, Canada) are hoping to better understand what happens during heart failure by determining what might be a more accurate predictor of the health problem that could potentially lead to better therapeutics.

The research, led by Robarts Research Institute scientists Robert Gros, PhD, and Marco Prado, PhD, along with graduate student Ashbeel Roy found that the heart is not only regulated by the nervous system but also by heart cells that regularly send messages to each other via neurotransmitter releases.

Gros explains through the study how heart activity is regulated by two nervous systems: the sympathetic and the parasympathetic. The sympathetic acts much like an accelerator in which the organ speeds up. On the other hand, the parasympathetic acts more like a stop, in which heart rate is decreased. However, when both systems encounter problems, it can eventually lead to heart failure.

"But the heart is not well innervated or in other words, there are very few nerves to control the heart. So we wanted to know how the signal from the nerve is communicated throughout the heart. A neuronal system is nerve-based but now we're talking about a non-neuronal system, which means it's not in any nerve tissue but found in the heart cells themselves," Gros, an associate professor in the Departments of Physiology & Pharmacology and Medicine at Western's Schulich School of Medicine & Dentistry and a scientist in the Vascular Biology Research Group at Robarts said, via a press release. "We've shown how the nerve sends a signal and individual heart cells pick up that signal; they can transduce that signal by the release of ACh from one cell to the next. It's the propagation of this signal that regulates the heart. Now we need to look at how this system changes in heart failure."

Robarts' worked in collaboration with scientist Vania Prado, Phd, in order to test the theory that mice engineered so that their heart cells exclusively could not release ACh. Yet they still had normal heart function under non-stressful conditions. However, when they exercised, the mice had a far greater increase in heart rate and it took longer for them to return to their pre-exercise heart rate compared to the control group.

These results suggest that heart cells derived from ACh may potentially boost parasympathetic signaling in order to counterbalance sympathetic activity.

Researchers hope this research may kick start new rules regarding the cells and their function in not just the heart but other organs as well.

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More information regarding the study can be found via the The FASEB Journal.