The mechanism of the relationship
One blow to two targets: diabetes and hypertension
As you know, diabetes mellitus and hypertension often go "in a bundle", but only recently it was possible to find out the reason for this mutual inclination. As it turned out, the regulation of blood sugar and blood pressure involves the same protein associated with the work of the sympathetic nervous system
Type 2 diabetes mellitus and arterial hypertension are very common diseases, and the number of such patients is only growing. At the same time, most prescribed medications are directed against the symptoms, not the causes of the disease. But the situation may change.
Recently, when studying the molecular biological features of the organism of laboratory rats serving as models of hypertension, scientists found a decrease in the activity of the gene encoding the GLP-1 protein (glucagon-like peptide-1 receptor) in carotid bodies located at the site of the carotid artery branching.
The GLP-1 protein is mainly known as a stimulator of pancreatic production of the hormone insulin, which controls blood glucose levels. As for carotid bodies, they are clusters of chemoreceptors sensitive to the concentration of oxygen, carbon dioxide and some other parameters in the blood. The nerve endings coming from them transmit information to the brain, which reacts by changing the work of the sympathetic nervous system, which regulates the work of internal organs. And increased activity of the sympathetic nervous system is known to be characteristic of patients with hypertension and type 2 diabetes.
Drugs that "activate" the GLP-1 receptor are already being used to treat diabetes. It is known that they also lower blood pressure, but the mechanism of this effect was unknown.
Using a similar drug, researchers in experiments on rats proved that activation of the GLP-1 receptor in carotid bodies suppresses pathological sympathetic reactions, including an increase in blood pressure.
As a result, it was possible not only to clarify the mechanism of action of GLP–1 receptor agonist drugs, but also to find a new therapeutic target for controlling sympathetic activity in diabetes mellitus and hypertension.
However, there is a nuance here: in rats on which experiments were conducted, the etiology of hypertension is mainly neurogenic, and it is with such a failure that GLP-1 receptor agonists are effective. In humans, the causes and mechanisms of hypertension are more diverse. For example, salt-sensitive hypertension develops in response to excessive consumption of table salt, and Goldblatt syndrome is secondary in kidney pathology.
Therefore, scientists will continue research on animal models of hypertension of a different etiology. But at the same time, the first human trials are also being planned to evaluate the possibility of using GLP-1 receptor agonists to treat two diseases at once.
Article by Pauza et al. GLP1R Attenuates Sympathetic Response to High Glucose via Carotid Body Inhibition published in the journal Circulation Research.
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