# The Role of the Acid Sensing Io Channel 1 in the Systemic Vasculature

> **NIH NIH F31** · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · 2020 · $24,177

## Abstract

PROJECT SUMMARY/ABSTRACT
 Acid sensing ion channel 1 (ASIC1) is a voltage-insensitive cation channel that has been shown to be
expressed in vascular smooth muscle and endothelial cells. However, little is known about the contribution of
ASIC1 to vascular resistance. Our preliminary data demonstrates that ASIC1 contributes to agonist-induced
vasodilation and endothelial cell Ca2+ influx in mesenteric arteries. Since the endothelium is a key regulator in
cardiovascular homeostasis and endothelial dysfunction is associated with several cardiovascular diseases, the
overall objective of this study is to identify the mechanisms by which ASIC1 contributes to endothelium-
dependent vasodilation and systemic vascular resistance. Based on our preliminary studies, our central
hypothesis is that ASIC1 contributes to cardiovascular homeostasis by mediating endothelium-dependent
vasodilation in the systemic circulation. We will identify the mechanisms by which ASIC1 contributions to
endothelial-dependent vasodilation and the role of ASIC1 to blood flow and blood pressure regulation with the
following specific aims:
Specific Aim 1: Determine the mechanism(s) involved in the activation of endothelial ASIC1.
 Hypothesis: Acetylcholine-induced release of arachidonic acid activates ASIC1 in the mesenteric
endothelium.
Specific Aim 2: Identify the mechanism by which ASIC1 mediates endothelium-dependent vasodilation.
Hypothesis: ASIC1 Ca2+ influx leads to the activation of small or intermediate conductance Ca2+ activated
potassium channels, thus mediating an endothelium-derived hyperpolarizing response.
Specific Aim 3: Determine the contribution of ASIC1 to cardiovascular homeostasis and disease.
Hypothesis: Endothelial ASIC1 contributes to both blood flow and blood pressure regulation, where a
loss of endothelial ASIC1 will lead to endothelial dysfunction and the development of hypertension.
 To test these hypotheses, we will use various techniques such as whole cell patch clamp
electrophysiology, sharp electrode membrane potential recording, and transient Ca2+ event recording upon
activation of ASIC1. We will also look at in vivo blood flow and blood pressure measurements in order to
understand the role of ASIC1 in cardiovascular homeostasis and blood pressure regulation. This project is
innovative in its investigation of a novel-signaling pathway involving the contribution of ASIC1 in agonist-induced
mesenteric vasodilation. These studies are significant because they are expected to virtually impact our
understanding of a novel mechanism that contributes to cardiovascular homeostasis and blood pressure
regulation. Ultimately, the training under this fellowship will facilitate the applicant’s next step into a postdoctoral
fellowship and overall career goal of becoming an independent scientist in cardiovascular physiology.

## Key facts

- **NIH application ID:** 9869704
- **Project number:** 5F31HL145836-02
- **Recipient organization:** UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR
- **Principal Investigator:** Selina M Garcia
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $24,177
- **Award type:** 5
- **Project period:** 2019-01-01 → 2020-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9869704

## Citation

> US National Institutes of Health, RePORTER application 9869704, The Role of the Acid Sensing Io Channel 1 in the Systemic Vasculature (5F31HL145836-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9869704. Licensed CC0.

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