Endothelial cell activation, reduced endothelial cell reparative capacity, and impaired endothelial-dependent vasodilation after anger provocation

Shimbo, Daichi; Rosenberg, Leah B.; Chaplin, William; Zhao, Shuqing; Golkin, Emma Goldensohn; Cholankeril, Matthew; Fu, Jie; Hong, Sang Bin; Jelic, Sanja; Burg, Matthew M.

The experience of anger increases the acute and long-term risks of incident cardiovascular disease (CVD) events [1] and [2]. The mechanism(s) whereby anger is associated with increased CVD risk remains to be fully characterized. One promising candidate mechanism is endothelial dysfunction. Endothelial dysfunction, as evidenced by impaired endothelial-dependent vasodilation, is an early pathogenic process underlying atherosclerosis development and CVD onset. More recent investigations have elucidated the cellular pathways underlying endothelial dysfunction. Endothelial cell (EC) injury can be assessed by measuring circulating levels of EC-derived microparticles (EMPs), which are phospholipid rich, submicron particles derived and released from the membranes of activated or apoptotic ECs [3]. In addition, the discovery of circulating, bone marrow-derived endothelial progenitor cells (EPCs) capable of EC repair and regeneration [4] suggests that endothelial function represents a balance between ongoing injury and repair.

We previously reported that anger provocation acutely impairs arterial vasomotion in apparently healthy individuals [5]. We conducted a study to examine the acute effects of anger provocation not only on arterial vasodilation but also on levels of EMPs and bone marrow-derived EPCs. To our knowledge, this is the first report concerning the adverse effects of anger provocation on cellular pathways underlying EC health.


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Also Published In

International Journal of Cardiology

More About This Work

Academic Units
Center for Behavioral Cardiovascular Health
Published Here
April 29, 2016