# Gustatory and interoceptive regulation of hypertension

> **NIH NIH F31** · UNIVERSITY OF FLORIDA · 2022 · $38,572

## Abstract

PROJECT SUMMARY
The overconsumption of sodium (Na+) is a major health problem in the U.S. and around the world,
having been linked to many health conditions, including hypertension—a major risk factor for
cardiovascular disease. While the relationship between Na+-intake and hypertension is widely
recognized, the mechanism(s) behind this relationship are not well understood. The proposed
experiments aim to delineate the mechanism(s) underlying this relationship by investigating
sensory systems that regulate Na+-taste/intake and blood pressure (BP). My preliminary studies
conducted in mice discovered that neurons within the nodose and petrosal ganglion that express the
angiotensin type 1a receptor (NPGAT1aR) send afferents to the nucleus of the solitary tract (NTS). The
NPG contains neurons that function as baroreceptors that sense blood pressure or as gustatory
afferents that transduce Na+-taste. Intriguingly, optogenetic excitation of afferents in the NTS arising
from NPGAT1aR significantly reduces blood pressure and Na+-intake. Moreover, mice overconsuming
NaCl solutions and rendered hypertensive via deliver of deoxycorticosterone acetate (DOCA-salt)
required greater frequencies of stimulation to lower blood pressure relative to normotensive mice.
Collectively, my preliminary results suggest that the NPGAT1aR send afferents to the NTS that mediate
the interoception of blood pressure and the perception of Na+-taste and the excitability of these neurons
can be used to study the etiology of hypertension that follows Na+ overconsumption. Accordingly, I
have developed the overall hypothesis that NPGAT1aR send afferents to the NTS that regulate blood
pressure and Na+-intake, and that AT1aR(s) on these neurons contribute to the development of DOCA-
salt hypertension. To confirm or refute this hypothesis, I will address the following aims. Aim 1 will use
neuroanatomical characterizations and optogenetic activation of NPGAT1aR afferents in the rostral and
caudal NTS to determine whether the connectivity and excitation of these afferents are sufficient to
alter Na+-intake and blood pressure under basal conditions and following depletion of blood volume.
Aim 2 will use Cre-LoxP system and virally-mediated gene transfer to selectively delete AT1aR(s) from
the NPG to determine whether these AT1aR are necessary for increased Na+-intake and decreased
baroreflex sensitivity that accompany the DOCA-salt model of hypertension. Collectively, these
experiments will shed light on gustatory and interoceptive integration in the brainstem to better
understand the relationship between Na+-intake and blood pressure regulation, thereby providing novel
insight that can be leveraged to develop treatments for hypertension.

## Key facts

- **NIH application ID:** 10388488
- **Project number:** 1F31HL162540-01
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **Principal Investigator:** Caitlin Marie Baumer Harrison
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $38,572
- **Award type:** 1
- **Project period:** 2022-01-01 → 2023-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10388488

## Citation

> US National Institutes of Health, RePORTER application 10388488, Gustatory and interoceptive regulation of hypertension (1F31HL162540-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10388488. Licensed CC0.

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