# Deciphering the autonomic regulation of inflammation and hypertension sensitization after psychological trauma

> **NIH NIH F31** · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · 2024 · $34,241

## Abstract

Project Summary
Post-traumatic stress disorder (PTSD) is a devastating psychiatric disorder that afflicts more than 7% of all
Americans across their lifespan. PTSD increases the risk for inflammatory cardiovascular diseases, such as
hypertension, but the etiology of this increased predilection for hypertension after psychological trauma is
unknown. Both PTSD and hypertension characteristically display increases in circulating levels of
norepinephrine, as well as alterations in T-lymphocyte-driven inflammation, evidence of autonomic system
alterations. T-Lymphocytes are highly reactive to norepinephrine, and we have previously reported that splenic
T-Lymphocytes exposed to sympathetic catecholamines, including norepinephrine, from the splenic nerve
secrete increased levels of interleukin 6 (IL-6) and interleukin 17A (IL-17A); pro-inflammatory cytokines which
have been mechanistically linked to the pathogenesis of hypertension. Furthermore, using an accepted model
of PTSD known as repeated social defeat, we have recently shown that denervating the splenic nerve, which
receives input from both sympathetic and parasympathetic systems and releases exclusively norepinephrine,
decreases splenic norepinephrine levels and concurrently levels of splenic T-Lymphocyte IL-6 and IL-17a.
Additionally, these observations and the hypertensive response to angiotensin II (Ang II) in animals
undergoing psychological trauma were ablated in mice lacking T-Lymphocytes, demonstrating these immune
cells are mechanistic in the sensitization to hypertension after trauma. To this end, I hypothesize that
psychological trauma alters autonomic signaling culminating in increased norepinephrine release through the
splenic nerve, by either sympathetic or parasympathetic pathways, that drives T-Lymphocyte inflammation
causing hypertension sensitization. In Specific Aim 1, I will determine the influence of central sympathetic and
parasympathetic signaling on inflammation and hypertension sensitization after psychological trauma using
chemogenetic technology to ablate each arm of the autonomic system upstream of the splenic nerve. In
Specific Aim 2, I will determine the effects of beta-adrenergic receptors mediating T-lymphocyte inflammation
and resulting hypertension sensitization after psychological trauma using genetic knockouts of specific beta-
adrenergic receptor signaling on T-lymphocytes. Additionally, with my goal of becoming an academic
researcher and educator at the R1 level focusing on autonomic and cardiovascular physiology, this project
provides the foundational training in autonomics, physiology, and mental health necessary to develop the
transferable skills to achieve my goal.

## Key facts

- **NIH application ID:** 10998535
- **Project number:** 1F31HL176172-01
- **Recipient organization:** TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR
- **Principal Investigator:** TATLOCK H LAUTEN
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $34,241
- **Award type:** 1
- **Project period:** 2024-09-01 → 2025-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10998535

## Citation

> US National Institutes of Health, RePORTER application 10998535, Deciphering the autonomic regulation of inflammation and hypertension sensitization after psychological trauma (1F31HL176172-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10998535. Licensed CC0.

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