The study showed that chronic stress can increase blood pressure by reducing the activity of a gene in the brain called STAT3. On the other hand, regular exercise helps restore this gene function, keeping blood pressure under control. This reinforces the importance of physical activity in protecting the heart and preventing hypertension.
Chronic stress is a significant risk factor for high blood pressure, or hypertension. When we are under stress for long periods, our body releases hormones such as cortisol and adrenaline, which increase the heart rate and the contraction of blood vessels.
This constant state of alertness can lead to a persistent increase in blood pressure, putting a strain on the heart and blood vessels. On the other hand, regular exercise is known to reduce the effects of stress on the body and help control blood pressure.
However, the exact mechanisms that explain why stress causes hypertension and how exercise can reverse this effect are still not fully understood. This study sought to investigate these relationships, focusing on the amygdala, a region of the brain involved in regulating stress and emotions.
To better understand this process, the researchers looked at how chronic stress and exercise affect blood pressure regulation at the molecular level.
They subjected one group of animals to three weeks of restraint stress (a method that simulates chronic stress) and another group to a daily exercise program. They then examined changes in genes expressed in the amygdala using a technique called microarray, which allows us to identify which genes are more or less active under different conditions.
From these analyses, they identified genes that could be involved in controlling blood pressure under stress. The results showed that chronic stress significantly increased the animals’ blood pressure.
However, those who exercised regularly had similar blood pressure levels to the control group, which did not experience stress. This suggests that exercise protects against the hypertensive effects of chronic stress.
In addition, the researchers found that stress reduced the expression of a gene called signal transducer and activator of transcription 3 (STAT3) in the amygdala, while exercise restored its levels to normal.
To better understand the role of this gene, the scientists investigated its location and function in neurons in the amygdala. They used a technique called small interfering RNA (RNAi) to block the expression of STAT3 and observed that this inhibition caused an increase in blood pressure.
This indicates that STAT3 plays an essential role in regulating blood pressure and may be directly involved in the body's response to chronic stress. On the other hand, other physiological markers related to blood pressure control, such as the baroreflex (a mechanism in the body that automatically adjusts blood pressure) and heart rate variability, were not affected by STAT3 inhibition.
This suggests that the effect of STAT3 on blood pressure occurs through another pathway, possibly through its influence on the emotional and autonomic response to stress.
In conclusion, this study revealed that the STAT3 gene in the amygdala plays an important role in controlling blood pressure and responding to chronic stress. When its activity is reduced by stress, blood pressure rises; when its activity is restored by exercise, blood pressure returns to normal.
These findings help explain how stress contributes to hypertension and reinforce the importance of physical exercise as an effective strategy for preventing and controlling high blood pressure.
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Potential role of signal transducer and activator of transcription 3 in the amygdala in mitigating stress-induced high blood pressure via exercise in rats
Keisuke Tomita, Ko Yamanaka, Thu Van Nguyen, Jimmy Kim, Linh Thuy Pham, Toru Kobayashi, Sabine S. Gouraud and Hidefumi Waki
Acta Physiologica. Volume241, Issue2 February 2025 e14274
Abstract:
Chronic stress elevates blood pressure, whereas regular exercise exerts antistress and antihypertensive effects. However, the mechanisms of stress-induced hypertension and preventive effects through exercise remain unknown. Thus, we investigated the molecular basis involved in autonomic blood pressure regulation within the amygdala. The effects of a 3-week restraint stress and daily voluntary exercise against stress on cardiovascular parameters and gene expression profiles in the amygdala were examined using a microarray method. Candidate genes were selected from differentially expressed genes; the localization of their expression within the central nucleus of the amygdala and their roles in cardiovascular regulation were examined using small-interfering RNA transfection and radiotelemetry. Chronic restraint stress caused an increase in blood pressure levels; however, with voluntary exercise, the blood pressure levels remained comparable to those of the controls. Compared with the controls, chronic restraint stress decreased signal transducer and activator of transcription 3 expression in the amygdala, whereas voluntary exercise improved its expression to normal levels. Immunohistochemical staining revealed the expression of signal transducer and activator of transcription 3 in neurons of the amygdala; inhibition of this expression using small-interfering RNA increased the arterial pressure. However, spontaneous baroreflex gain and low- and high-frequency components of heart rate variability remained unaffected by the inhibition of signal transducer and activator of transcription 3. In the amygdala, signal transducer and activator of transcription 3 regulates the blood pressure levels and is possibly involved in blood pressure elevation in response to chronic stress and its improvement by voluntary exercise.
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