High-salt diet leads to cardiovascular diseases: Here’s how

These neurons play an important role in allowing our bodies to maintain a healthy homeostasis by using this skill set to efficiently remove excess salt, say scientists. the amount we consume in an unhealthy meal.

But scientists at the Medical College of Georgia and Georgia State University also say that the chronically high-salt diet most Americans consume can turn this system against us, leading to an increase in blood sugar levels. This nerve cell, which continues to produce this hormone vasopressin, constricts blood vessels and increases the risk of common cardiovascular metabolic diseases such as high blood pressure and heart disease.

New $2.7 million new investigator grant (RHL162575A1) from the National Institutes of Health allows scientists to delve deeper into how cardiovascular metabolic diseases occur and identify new therapeutic targets for them.

The large neurons in the nuclei of the hypothalamus near the base of the brain secrete oxytocin, a hormone important in the reproductive system, as well as vasopressin, known as the antidiuretic hormone because it actually helps the body keeping fluids down, which can help with dilution Dr. Jessica A. Filosa, a neurophysiologist in the MCG Department of Physiology, says excess salt is left in the body to be excreted in the urine.

“We are looking at how the brain perceives high salt intake and how it responds to that high salt intake to effectively correct the disturbance and regain homeostasis.” Filosa said.

She and Dr. Javier E. Stern, director of the GSU Center for Neuritis and Cardiovascular Diseases, are both PIs in the new grant.

They found that salt intake increased vasopressin-producing neurons, which increased the constriction of blood vessels and decreased local blood flow. More commonly when nerve cells are active, blood flow to them increases, in a process known as neurovascular coupling. This helps ensure functioning nerve cells get the oxygen and nutrients they need to sustain increased activity.

In the epithelium, however, Stern, Filosa and their colleagues have shown that high vasopressin neuronal activity induces apparently self-generating and persistent contraction of a large network of neurons. blood vessels directly nourish them. The researchers also show that local hypoxia – an oxygen supply considered inadequate to maintain homeostasis – is one of the mechanisms that causes vasopressin neuronal activity to be stimulated. more. It is a form of inverse neurovascular coupling.

“Your body wants to stay in balance,” Filosa said. “Anytime you do something to your body or something happens to you that deviates from that balance, the homeostatic processes kick in and (at least try to) restore it.” balance.” In this case, excess salt is responsible for activating homeostasis.

But the process turns out to be a problem that instead contributes to high blood pressure and other problems that can occur when high salt intake becomes chronic for most of us: 90% of people Americans 2 years of age and older consume too much sodium, according to the Centers for Disease Control and Prevention, averaging more than 3,400 milligrams per day compared with the recommended 2,300 milligrams.

The new funding enables studies in both tissues and animal models developed by Stern to further understand the specific mechanisms and signals and show how that results in reduced blood flow in the cell region. vasopressin neurons increase rather than decrease their activity. And, what happens to this abnormal response in the face of conditions like heart failure?

They also wanted to know if they constricted the blood vessels for the first time, whether it would still respond strangely to increased neuronal activity. This kind of insight will help them better analyze the path. They already knew that a lack of oxygen makes the environment more acidic, and that these neurons have acid-sensing ion channels, or ASICs, which means that a low pH can activate ASIC channels and increase the activity of these neurons. neuron. That could mean chronic high salt consumption, which leads to increased blood pressure, remodeling of blood vessels and enhanced constriction, which also works in this direction to further stimulate nerve cells to continue releasing vasopressin.

Another piece of the puzzle is astrocytes, the astrocytes that support neurons and often ramp up their game when neurons are more active. But in this region, the high salt levels prompt the astrocytes to retract their course, which is likely to worsen the situation since one of the astrocytes’ many jobs is to remove the signals from the astrocytes. stimulus signals from where these neurons sit to keep them from becoming overactive.

They are also exploring further early evidence that another graft, the slow buildup of natural, potent nitric oxide that dilates blood vessels that hypoxia also causes, could be a mechanism for weight loss. homeostasis for these overactive neurons. There are many potential sources for nitric oxide nearby, including the nerve cells themselves, the supporting astrocytes, and potentially the endothelial cells lining blood vessels.

But Filosa notes that in cardiometabolic disease, impaired nitric oxide signaling could mean that the mechanism for shutting down vasopressin neurons is impaired, something they will also explore in a model of heart failure mine.

One of the other questions they want to answer is if you have too much vasopressin in the upper nuclei, does that decrease blood flow to other areas of the brain, including areas that need more blood to function? more active.

“You start with a really quick process that’s supposed to correct imbalances in the body and it does as long as you’re healthy.” she speaks. But if anything is disrupted, such as too little nitric oxide or too much vasopressin, it instead leads to an ill-reactive and excitable vasopressin neuron, setting off a cycle vicious and unhealthy.

“I think the take-home message here is that we have a very sophisticated system in this part of the brain that can rapidly recover from disturbances, like with a high-salt meal, and you want to keep the system healthy. that system is healthy,” Filosa said.

Work began in Filosa’s lab with former graduate student Dr. Wenting Du working in brain slices and discovering that if you stimulate vasopressin neurons, the blood vessels around them constrict. , it’s obviously a local action. When the scientists blocked the activity of the nerve cells, the blood vessel constriction did not occur.

In collaboration with Dr. Colin Brown, a hypothalamic researcher at the Center for Neuroendocrinology at the University of Otago Research Center in New Zealand, Stern has developed an in vivo approach to imaging the viral nucleus. of the hypothalamus allows scientists to see if they’ve found something first. The response to salt administration to these ex vivo neurons also occurred in the intact brain. With the developed in vivo neuroimaging technique, the scientists watched in real time as salt promoted sustained increases in vasopressin neuronal activity and constriction of the blood vessels of the uterus. super buffer level. In addition, they observed that the contraction was sufficient to induce hypoxia in the area and increase neuronal activity.

As part of a large collaborative effort, Dr. Stern, Filosa, Brown, Du and others reported this unusual reaction late last year in the journal Cell Reports. Stern commented at the time, lower blood flow in other brain regions, like the cerebral cortex, in response to stimulation is often associated with medical conditions, like Alzheimer’s or stroke. There are still other brain regions that use this rather unorthodox approach to increase neuronal activity, Filosa said.

The irony is that this hypoxia-induced increase in neuronal activation is caused by the fact that the supraneuronal nucleus has an enormous network of blood vessels that supply neurons that are strangely normal. have the ability to combat hypoxia, a fact that has always left scientists scratching their heads.

Source: Eurekalert

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