Related Experiment Videos
Endothelial dysfunction in response to psychosocial stress in monkeys
W B Strawn1, G Bondjers, J R Kaplan
1Arteriosclerosis Research Center, Bowman Gray School of Medicine, Winston-Salem, N.C.
Circulation Research
|May 1, 1991
Summary
Social disruption in monkeys causes sympathetic arousal and endothelial dysfunction. Beta-blocker treatment prevented these negative effects, highlighting potential cardiovascular benefits.
Area of Science:
- Cardiovascular Science
- Neuroendocrinology
- Primate Research
Background:
- Social disruption is a significant stressor.
- Stress impacts cardiovascular health through the sympathetic nervous system.
- Endothelial dysfunction is an early marker of cardiovascular disease.
Purpose of the Study:
- To investigate the impact of social disruption on endothelial integrity in cynomolgus monkeys.
- To determine if beta-adrenergic blockade mitigates stress-induced endothelial changes.
Main Methods:
- Male cynomolgus monkeys (Macaca fascicularis) underwent a social disruption protocol.
- Half received metoprolol (beta-blocker) prior to and during social housing.
- Vascular segments were analyzed for endothelial markers (IgG, replication) and lipoprotein levels.
Main Results:
- Social disruption increased heart rate and sympathetic arousal in untreated monkeys.
- Untreated monkeys showed greater immunoglobulin G incorporation and endothelial cell replication at aortic branch sites.
- Metoprolol treatment attenuated heart rate increases and reduced endothelial cell replication.
Conclusions:
- Social disruption induces sympathetic arousal and endothelial dysfunction in monkeys.
- Beta-adrenergic blockade with metoprolol can prevent these stress-related vascular changes.
- Findings suggest a link between social stress, the nervous system, and cardiovascular health.