# Project 8 - Autonomic regulation of coronary blood flow in the superior and inferior sinoatrial node

> **NIH NIH P20** · UNIVERSITY OF NEVADA RENO · 2024 · $249,053

## Abstract

Project 8 Abstract
The sinoatrial node is the origin of organized and rhythmic electrical depolarizations in the heart. After leaving
the sinoatrial node, depolarizations spread throughout the atrium and ventricles via the atrio-ventricular node
and specialized conduction pathways to initiate excitation-contraction coupling of cardiomyocytes. This highly
organized pattern of events is critical for blood to be pumped throughout the pulmonary and systemic
circulations. Therefore, the sinoatrial node is critical for the initiation of each cardiac cycle. To sustain the
constant diastolic spontaneous depolarizations in the sinoatrial node, blood is delivered to the node via the
right coronary artery. Although many groups have investigated the mechanisms responsible for nodal
pacemaking, we continue to have a very limited understanding of how blood flow is regulated in the sinoatrial
node during either resting or elevated physiological conditions (i.e., exercise). Adequate perfusion of the node
is critical since clinical evidence suggests that damage or blockage of the sinoatrial nodal artery is pro-
arrhythmogenic. Previous studies indicate that there are differences in microvascular density between the
superior and inferior regions of the sinoatrial node, however the significance of this is unclear. The overarching
goal of this project is to determine how blood flow is regulated during sympathetic nervous system activation
and how this regulation is affected during disease such as heart failure. First, we plan to investigate the spatial
relationship between sympathetic nerves and cell types involved in mediating vascular resistance (i.e.,
vascular smooth muscle cells, endothelial cells and pericytes) to determine where the effects of sympathetic
activation are mediated. Next, we will isolate microvasculature from the sinoatrial node and elucidate the effect
of sympathetic activation to determine whether the superior and inferior sinoatrial node artery responds
differentially to nerve activation. Lastly, we will investigate how heart failure in the mouse causes changes in
the microvascular density and response to sympathetic stimulation. This project will serve as a basis for future
studies by dissecting the key components of blood flow regulation in the sinoatrial node.

## Key facts

- **NIH application ID:** 10850207
- **Project number:** 2P20GM130459-06A1
- **Recipient organization:** UNIVERSITY OF NEVADA RENO
- **Principal Investigator:** Nathan Grainger
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $249,053
- **Award type:** 2
- **Project period:** 2019-01-01 → 2029-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10850207

## Citation

> US National Institutes of Health, RePORTER application 10850207, Project 8 - Autonomic regulation of coronary blood flow in the superior and inferior sinoatrial node (2P20GM130459-06A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10850207. Licensed CC0.

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