How Stress Causes Clogged Arteries
Biologists for the first time explained the link between stress and a heart attack
Copper news based on ScienceNOW materials: How stress can clog your arteriesBiologists from the Harvard School of Medicine for the first time revealed the physiological mechanism that causes the link between chronic stress and acute dysfunction of the cardiovascular system.
As it turned out, prolonged stress triggers a cascade of reactions in the body that lead to excessive production of leukocytes – protective cells of the immune system that accumulate in the arteries and lead to the formation of complicated atherosclerotic plaques prone to rupture and formation of blood clots, which eventually leads to a heart attack or stroke. The work was published in the journal Nature Medicine (Heidt et al., Chronic variable stress activates hematopoietic stem cells).
Previous studies of the group led by Matthias Nahrendorf have shown that under chronic stress, atherosclerotic plaques contain, in addition to fats, cholesterol and calcium, significantly increased levels of two types of leukocytes compared to normal ones – monocytes and neutrophils. This discovery, which allowed them to suggest a link between prolonged stress and hyperactivity of the immune system, was made by Narendorf and his colleagues during the observation of 29 doctors and nurses working in the intensive care unit.
To confirm their assumption, the scientists turned to a mouse model of chronic stress. For six weeks, the animals were placed in various stressful situations for them. In comparison with the control group of mice, mentally traumatized animals, as well as humans, had an increased content of monocytes and neutrophils in the blood.
Investigating the causes of leukocytosis, Narendorf and his colleagues came to the conclusion that the biological mechanism leading to it is as follows: prolonged stress exposure is associated with excessive release of the hormone norepinephrine into the blood. The hormone, as scientists have found out, binds to the beta3 protein, a surface protein of hematopoietic stem cells, which, in turn, causes their excessively rapid proliferation (division) and, accordingly, excessive production of protective immune cells.
Hematopoietic (hematopoietic) stem cells are bone marrow cells that have the ability to intensively divide, from which, thanks to differentiation and maturation, all types of blood cells are obtained, which ensures its constant renewal.
"It makes sense in the case of short–term stress - the overproduction of leukocytes in a situation of sudden danger, the body is preparing for possible injury in battle. However, chronic stress is a completely different story, there is no wound or infection, and the excess of immune cells begins to work to the detriment," explained Narendorf.
Scientists have found that mice living under stress develop complicated atherosclerotic plaques in the vascular lumen due to active migration and accumulation of leukocytes, which are prone to rupture and formation of blood clots, which are the greatest risk factor for stroke or myocardial infarction in humans. Blocking of beta3 receptors on the surface of hematopoietic cells led to a decrease in the number of complicated plaques and a decrease in the number of active immune cells in them, which allowed the authors to call this protein a link between stress and atherosclerosis.
The disclosure of the mechanism explaining why chronic stress is a risk factor for cardiovascular diseases opens up new opportunities for their therapy and prevention, the journal Science quotes the opinion of biologist Lynn Hedrick from the La Jolla Institute for Allergy and Immunology (San Diego, California). The development of a drug that specifically blocks beta3 receptors will interrupt the chain reaction linking chronic stress, norepinephrine production, activation of hematopoietic stem cells, excessive production of leukocytes and the formation of atherosclerotic plaques, Hedrick believes.
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