Beta-Blocker Influences on Inflammatory and Neural Responses to Stress

Cardiovascular Disease Clinical Trial

Official title: Beta-Blocker Influences on Inflammatory and Neural Responses to Stress

Status Not yet recruiting

Clinical Trial Summary

The purpose of this study is to map the neural and molecular mechanisms underlying psychological stress-induced changes in inflammation which could reveal new targets for intervention to reduce the risk of cardiovascular disease.

Clinical Trial Description

The proposed work will conduct a mechanistic clinical trial utilizing the non-selective beta-adrenergic receptor blocker propranolol to examine the role of beta-adrenergic signaling in shaping neural and inflammatory responses to stress. The investigators will focus on beta-adrenergic signaling given seminal pre-clinical work showing that this molecular pathway is an important driver of stress-related increases in inflammation, and initial human neuroimaging work showing that beta-blockade leads to changes in neural responses to negative stimuli. Here, the investigators will bring these two previously disparate lines of work together to determine how experimentally blocking one critical stress-signaling pathway shapes neural activity and inflammatory responses to stress. In doing so, the investigators will be advancing knowledge by mapping mechanisms (i.e., beta-adrenergic signaling), offering methodological improvements (i.e., moving beyond correlation to using pharmacological manipulations to provide causal evidence), and identifying intervention targets (i.e., the neurocognitive systems that shift activity/connectivity in response to beta-blockade). In sum, the work proposed herein is significant because it will address the mechanisms by which one critical risk factor, psychological stress, may ultimately lead to cardiovascular disease via inflammation. The proposed study also offers significant methodological improvements over past work by using neuroimaging to identify neurocognitive pathways, and pharmacology to provide causal experimental evidence to move us beyond correlation. Finally, this project is significant because it could provide insight into novel targets for future interventions. ;

Related Conditions & MeSH terms

• Cardiovascular Disease
• Cardiovascular Diseases

• NCT number: NCT06263452
• Study type: Interventional
• Source: University of North Carolina, Chapel Hill
• Contact: Madison K Tarkenton, BA
• Phone: 9197102168
• Email: mktark@unc.edu
• Status: Not yet recruiting
• Phase: Phase 4
• Start date: March 2024
• Completion date: March 2026