Catecholamines mediate stress-induced increases in peripheral and central inflammatory cytokines.
J D Johnson, J Campisi, C M Sharkey...
https://pubmed.ncbi.nlm.nih.gov/16165282/Actively Recruiting
Led by University of North Carolina, Chapel Hill · Updated on 2025-10-29
120
Participants Needed
1
Research Sites
N/A
Total Duration
Researchers are investigating how psychological stress leads to changes in inflammation that may increase the risk of cardiovascular disease. This study focuses on understanding the role of beta-adrenergic signaling, a molecular pathway involved in stress responses, by examining how blocking this pathway affects brain activity and inflammatory responses. The study combines neuroimaging and pharmacological methods to provide new insights into stress-related mechanisms and potential intervention targets. Participants will receive either a single oral dose of 40 mg propranolol, a non-selective beta-adrenergic receptor blocker, or an identical placebo capsule. The study uses a randomized, triple-blind design to compare the effects of propranolol versus placebo on neural and inflammatory responses to social stress. This design aims to causally link beta-adrenergic signaling with changes in inflammation and brain activity. During the study, participants will undergo social stress tasks while researchers measure changes in inflammatory markers, such as interleukin-6 and inflammatory gene expression, at specified times after drug administration and stress exposure. The study includes assessments of neural responses via neuroimaging and careful monitoring of participants health and adherence. The total participation period extends from baseline measurements through 90 minutes post-stress to capture these responses.
CONDITIONS
Beta-Blocker Influences on Inflammatory and Neural Responses to Stress
J
Jonathan Bunting, BS
K
Keely A Muscatell, PhD
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University of North Carolina, Chapel Hill
Lead Sponsor
National Heart, Lung, and Blood Institute (NHLBI)
Collaborating Sponsor
This table compares participation in this trial with other options available for this condition. The information is drawn from published research and the trial’s study details and is provided for educational purposes only.
| Factors | Propranolol | Placebo |
|---|---|---|
| What it is | An encapsulated tablet of propranolol, a non-selective beta-adrenergic blocker, administered to participants prior to a standardized social stress task in the laboratory. | A visually identical encapsulated inert tablet (placebo) given under the same laboratory settings for controlled comparison against propranolol. |
| Role in trial | Investigational arm receiving active drug to assess its acute impact on inflammatory and neural response to social stress in healthy volunteers. | Comparator arm receiving placebo; serves as the control to isolate the pharmacological effect of propranolol on measured outcomes during social stress. |
| Primary use or purpose | To evaluate whether propranolol modifies biological and neural responses, such as inflammatory markers (IL-6) and brain activity, during acute social stress among healthy young adults. | To serve as a reference condition, allowing the isolation of changes caused by active propranolol from those associated with social stress itself or other non-specific effects. |
| How it is given | A single encapsulated tablet is taken before participants complete a laboratory social stress task, with matching procedures for timing and dose as defined by the trial protocol. | A single matching placebo tablet is administered identically before the laboratory stress task. |
| Evidence status | A meta-analysis and randomized controlled trials indicate that beta-blockers such as propranolol can modulate some inflammatory responses to acute mental or social stress in humans, but the effects are inconsistent and may depend on the specific marker and study design. Use in healthy volunteers in a single experimental session is investigational and not intended for clinical therapy. | Placebo is an inert comparator and does not exert physiological effects on stress or inflammation. In experimental human studies, placebo-controlled designs are considered the gold standard to test the specific effects of interventions. |
| Important limitations | Findings from acute, short-term administration in young, healthy participants may not generalize to patients with cardiovascular disease or chronic stress. The protocol does not test repeated or clinical dosing, and observed biomarker changes may not reflect clinical benefit. | As an inert tablet, the placebo arm only controls for non-specific study effects. Results in a laboratory environment with healthy volunteers do not indicate clinical responses to stress in real-world or patient populations. |
Disclaimer: This comparison is created with the help of artificial intelligence(AI) and may contain errors or missing information. It is not medical advice and does not mean one option is better or safer than another. Clinical trials are still being studied, and joining a trial is your choice. Please consult your healthcare professional before making any decisions.
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Duration - 2 to 4 weeks
Participants are screened for eligibility to participate in the trial.
1 visit (in-person)
Duration - Single day
Participants receive a single oral dose of either propranolol or placebo to study its effects on inflammatory and neural responses to stress.
1 treatment visit with assessments before and after dosing
Study Type
INTERVENTIONAL
Masking
TRIPLE
Allocation
RANDOMIZED
Model
PARALLEL
Primary Purpose
BASIC_SCIENCE
Number of Arms
2
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https://pubmed.ncbi.nlm.nih.gov/26256574/University of North Carolina, Chapel Hill
Lead Sponsor
National Heart, Lung, and Blood Institute (NHLBI)
Collaborating Sponsor