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Endogenous opioids modulate the cardiovascular response to mental stress
M Morris1, P Salmon, H Steinberg
1Department of Psychology, University College London.
Psychoneuroendocrinology
|January 1, 1990
Summary
Endogenous opioids inhibit cardiovascular responses to mental stress. Naloxone, an opiate antagonist, enhanced heart rate during stress, indicating opioid system
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Endocrinology
Background:
- The cardiovascular system's response to mental stress involves complex hormonal and neural pathways.
- Endogenous opioids are implicated in modulating physiological responses, including stress.
- Understanding the role of endogenous opioids is crucial for managing stress-related cardiovascular conditions.
Purpose of the Study:
- To investigate the role of endogenous opioids in mediating cardiovascular, hormonal, and psychological responses to mental stress.
- To determine if naloxone, an opiate antagonist, alters the physiological and psychological effects of acute mental stress.
Main Methods:
- Two controlled studies were conducted involving mental stress tasks and non-stressful control tasks.
- Participants received either naloxone (8 mg) or a saline placebo in a single-blind or double-blind manner.
- Cardiovascular (heart rate, blood pressure), hormonal (epinephrine, norepinephrine, cortisol, ACTH), and psychological (anxiety) measures were collected.
Main Results:
- Naloxone significantly enhanced the heart rate response to mental stress but did not affect blood pressure or anxiety levels.
- Plasma levels of epinephrine and norepinephrine were not altered by naloxone during stress.
- Naloxone increased plasma cortisol and ACTH levels irrespective of the task (stressful or control).
Conclusions:
- An endogenous opioid mechanism appears to inhibit the cardiovascular response, specifically heart rate, during mental stress.
- Opioid antagonism with naloxone unmasks or enhances the heart rate reactivity to stress.
- These findings highlight a novel inhibitory role for endogenous opioids in the acute stress response.