# Lipid emulsion attenuates vasodilation by decreasing intracellular calcium and nitric oxide in vascular endothelial cells

**Authors:** Ling Chen, Hui Bai, Jing Zhao, Panpan Zhang, Xinhua Zhang, Dezhi Kong, Changzheng Dong, Wei Zhang

PMC · DOI: 10.1016/j.heliyon.2024.e37353 · 2024-09-03

## TL;DR

Lipid emulsion reduces vasodilation by lowering calcium and nitric oxide in vascular cells, which could explain its effect on blood vessels.

## Contribution

This study identifies novel mechanisms by which lipid emulsion reverses vasodilation through intracellular calcium and nitric oxide modulation.

## Key findings

- Lipid emulsion pretreatment suppresses ATP-induced calcium elevation in endothelial cells.
- LE reduces intracellular calcium concentration and nitric oxide production in endothelial cells.
- The effect of LE persists even after extracellular calcium is removed.

## Abstract

Lipid emulsion (LE), a widely used parenteral nutrition, exhibits a well-documented ability to reverse the vasodilatory effects induced by acetylcholine in blood vessels. However, the specific mechanisms underlying this action are not yet fully understood. This study aimed to elucidate the mechanism by which LE reverses vasodilation in vitro through dose-response curve experiments, calcium imaging, and fluorescence assays. The results revealed a significant attenuation of acetylcholine (Ach)-induced vasodilation in rat thoracic aortic rings following LE exposure. In human aortic endothelial cells, pretreatment with LE significantly suppressed ATP-induced calcium elevation. This suppression persisted even after elimination of extracellular calcium with a calcium chelator. Moreover, LE pre-exposure reduced the intracellular calcium concentration ([Ca2+]i) elevation in endothelial cells following cyclopiazonic acid (CPA) treatment, suggesting enhanced endoplasmic reticulum (ER) calcium reuptake. Additionally, nitric oxide (NO) fluorescence assays showed a decrease in NO production upon ATP stimulation post-LE pretreatment of endothelial cells. Taken together, these results indicate that the reversal of vasodilation by LE may involve enhanced ER calcium uptake, leading to a reduction in intracellular calcium concentration and suppression of NO (key vasodilatory agent) synthesis.

Schematic of the lipid emulsion (LE) effect on vascular response.Image 1

## Linked entities

- **Chemicals:** acetylcholine (PubChem CID 187), ATP (PubChem CID 5957), cyclopiazonic acid (PubChem CID 54682463), nitric oxide (PubChem CID 145068)
- **Species:** Rattus norvegicus (taxon 10116), Homo sapiens (taxon 9606)

## Full-text entities

- **Chemicals:** NO (MESH:D009569), calcium (MESH:D002118), Ach (MESH:D000109), ATP (MESH:D000255), Ca2+ (-), CPA (MESH:C000543)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11408769/full.md

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Source: https://tomesphere.com/paper/PMC11408769