Anger disrupted endothelium-dependent vascular dilation
An experiment by American scientists has shown that provoked anger reduces the degree of vascular dilation - vasodilation - due to abnormalities in endothelial cells. As reported in the Journal of the American Heart Association, anxiety and depressed mood did not affect the state of the endothelium.
Since the middle of the last century, cardiologists have noted that people with a pattern of behavior based on competition, workaholism and aggression have an increased risk of cardiovascular disease. Scientists have conducted a fair amount of research on the relationship between psychosocial factors and associated cardiovascular disease. Thus, experiencing negative emotions may be associated with an increased risk of cardiovascular disease regardless of traditional risk factors. One of the most studied negative emotions associated with cardiovascular disease is considered to be anger, but the mechanisms by which the experience of anger affects the pathogenesis of, for example, atherosclerosis, are not well described.
The endothelium is known to act as a key regulator of vascular homeostasis. Endothelial cells play an important role in maintaining vascular tone and integrity of blood vessels. Endothelial dysfunction is considered the starting and underlying mechanism for the development of atherosclerosis and cardiovascular disease. Several studies have demonstrated that mental workload, such as arithmetic operations in the mind or public speaking, impairs endothelium-dependent vasodilation. However, data on the effects of provoked anger, anxiety or sadness on human health are scarce.
A team of scientists led by Daichi Shimbo of Columbia University studied the biochemical effects of provoked anger, anxiety and sadness on endothelial cells. The study included 280 adults who took part in an experiment. The participants were seated in a comfortable chair where they had their blood pressure and reactive hyperemia index, which reflects the degree of endothelium-dependent vasodilation, measured. They also had an intravenous catheter inserted into the ulnar vein of the dominant arm. Volunteers were asked to relax for 30 minutes, during which time they were not allowed to talk, use phones, read any documents, or sleep; this condition was taken as baseline.
After baseline scores were obtained, participants were assigned to one of four groups: anger, anxiety, sadness, and neutral condition. Anger and anxiety were elicited as follows: the participant was asked to recall relevant personal memories that would elicit either anger or anxiety for eight minutes. Sadness was elicited by reading sadness-inducing texts for eight minutes. In the "neutral group," participants were asked to count aloud from 1 to 100 over and over until eight minutes had passed. After completing the task, participants sat quietly in a chair and were not allowed to talk, use phones, read any documents, or sleep.
Analysis of the data showed that compared to the neutral condition, anger statistically significantly reduced the reactive hyperemia index, reflecting impaired endothelium-dependent vasodilation 40 minutes after recalling anger (p = 0.007). When assessing all other conditions, the researchers found no statistically significant association between anxiety and sadness and impaired endothelium-dependent vasodilation. There were also no changes in endothelial progenitor cell concentrations.
The scientists reach the interim conclusion that not all negative emotions may have the same negative impact on cardiovascular disease risk. Future studies of the mechanisms underlying the link between anger and endothelial dysfunction should therefore identify the specific molecular pathways of anger's effects on this risk.