Cells and the body’s response to chemical cues: the role of the parietal and posterior parietal membranes in the regulation of heart rate and breathing
By Robert B. MolloyPublished February 16, 2019 2:12pmThis article first appeared in The Atlantic.
It has been suggested that cells, like our eyes and muscles, play a crucial role in regulating body temperature and heartbeat.
These cells, known as thermoreceptors, detect and respond to the body temperature, and regulate breathing.
But the paracentral membrane, which surrounds the heart, is not the only membrane in the body that can be affected by chemical cues.
In recent years, researchers have identified receptors for chemical cues that are released in response to the presence of toxins, such as ammonia or other acids.
This has led to the development of a new class of molecules that are able to interact with the paracervical membrane and regulate its functions.
Now, a team of researchers at the University of Bristol has developed a molecule that can activate the parabecular membrane and stimulate the heart to beat more rapidly.
The team is currently working to develop a similar molecule that could help the heart beat more quickly in the event of an acute or chronic infection.
In their study, published in Nature Communications, the researchers tested the ability of a molecule called SNS-2 to activate the heart in a rat model.
The researchers found that the SNS molecule was able to stimulate heart rate, blood pressure and oxygen saturation to a level that was higher than those observed in a control group of rats.
In other words, when injected into the heart and given to the rats, the SNT-2 molecule caused a dramatic increase in heart rate.
“We showed that SNS2 could activate the cardiac pacemaker,” said lead researcher, Dr. Peter Diamandis.
“We also demonstrated that this could occur when given to other organs, such that it would be able to inhibit the cardiac function of an entire group of heart cells.”
In the study, the team injected SNS1 into the rats’ thoracic arteries and measured the response.
They found that cardiac activity was increased by about 20% in the rats given SNS, while heart rate was also increased by 20%.
The team also found that when SNS was administered to the hearts of the rats with acute or a chronic infection, cardiac activity increased by 30% and heart rate increased by 50%.
Dr. Diamands said the results indicate that the molecules SNS and SNT2 work in a similar way.
“The idea that you can induce an effect on cardiac function and cardiac function in an organism that is not a heart is a bit of a leap,” said Dr. Dias.
“It seems like a bit more work to make that leap.”
While the heart does not have a functional paracardial layer that would protect the heart from toxic substances, the human body does have a layer of cells called the parafaculum that regulates temperature and respiration.
When the paraffaculum gets too cold, for example, it can damage the heart.
When the temperature of the body rises, this layer of blood cells secrete a chemical called hypothermia.
This causes the heart muscle to contract, which causes blood to clot.
When blood clotting slows, the heart contractions become more pronounced, leading to more rapid heart rate growth.
Dr. Murch said that this phenomenon can happen in any animal.
“Any time there’s an increase in the temperature, the blood cells start secreting a molecule,” she said.
“They release that molecule, and this is what causes the temperature to rise, and then that causes the contraction of the heart.”
The researchers are now working to identify the exact molecules that activate these processes and how the effects occur.
“What we’re trying to figure out is what are the molecular mechanisms that are involved in regulating these functions in the paraventricular zone, and what are these molecules that we can make to trigger these effects in an animal?” said Dr Dias, “and what would that be like to use in humans?”
The work is supported by the National Institutes of Health (grant no.
The American Heart Association, the American Association of Blood Banks and the European Blood and Transplant Society also contributed to this study.
Source The Atlantic