Endothelium derived relaxation factors reduce sulfur dioxide-induced aortic relaxation

Omar A M Al-Habib,Abbas B Q Salihi

doi:10.4236/ojmip.2013.34023

Omar A M Al-Habib, Abbas B Q Salihi

Open Access

https://doi.org/10.4236/ojmip.2013.34023

Copy DOI

Abstract

The endothelium plays a key role in the control of vascular patency and tone. Thus, the main objective of the study was to determine the role of endothelium and its derived relaxation factors in mediating relaxation of rat thoracic aorta, in response to sulfur dioxide (SO2) derivatives “1:3 M/M sodium bisulfite (NaHSO3) and sodium sulfite (Na2SO3)” using PowerLab tissue bath system. Endothelial denudation enhanced relaxation responses of SO2 derivatives with an IC50 of 6.11 mM as compared to control rings with an IC50 of 6.21 mM, as well as the maximum relaxation (Emax) was increased from 62.026% ± 6.527% to 83.13% ± 14.755%. Furthermore, the relaxation responses to SO2 derivatives in aortic rings were significantly enhanced by indomethacin, clotrimazole and methylene blue with IC50’s of 4.8 mM, 5.33 mM and 4.01 mM, and Emax were raised to 101.1% ± 6.537%, 66.92 ± 7.538 and 104.68 ± 3.575, respectively. Meanwhile, L-NAME did not alter dose-dependent relaxation of SO2 derivatives in comparison to control aortic rings. The results of this study had shown that endothelium denudation and blocking of endothelium derived-relaxation factors enhanced vasodilator effect of SO2; this may clarify the role of endothelium in the vasodilatory mechanism of SO2.

Highlights

The vascular endothelium is strategically located at the interface between the circulating blood and vessel wall, providing a permeability barrier to the movement of cell metabolites and nutrients, while allowing the transfer of electrical signals within the intact tissue [1]
Inclusion of aortic rings with L-NAME did not alter dilation from control, this response tended towards significance in precontracted rings with indomethacin, clotrimazole and methylene blue with an IC50’s of 4.801 mM, 5.331 mM (4.868 to 5.795) and 4.011 mM (3.846 to 4.176), and Emax were increased to 101.1% ± 6.537%, 66.92 ± 7.538 and 104.68 ± 3.575 respectively, as shown in (Figures 2-6 and Table 1)
The results of the present study demonstrated that removal of functional endothelium increased the relaxation response to SO2 only at high dose (7 mM), indicating that vasorelaxation of SO2 may be inhibited by substances released by endothelium

Summary

Introduction

The vascular endothelium is strategically located at the interface between the circulating blood and vessel wall, providing a permeability barrier to the movement of cell metabolites and nutrients, while allowing the transfer of electrical signals within the intact tissue [1]. Endothelial cells synthesize and release various factors that modulate in short terms vascular tone. Inhaled SO2 is hydrated to produce sulfurous acid in the respiratory tract, which subsequently dissociates to form its derivatives, bisulfite and sulfite (1:3 M/M in neutral fluid). The derivatives can be absorbed into the blood or other body fluids [4]. Bisulfite/sulfite enters the body via foods, beverages and drugs, because of sulfiting agents, such as SO2, metabisulfite, NaHSO3, and Na2SO3 [5]. Vasodilatory effect of SO2 derivatives on isolated rat aortic rings first reported by Meng and his team in 2005, the exact mechanism of vasodilatation is still unknown [7]

Objectives

Methods

Results

Conclusion