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1 Biomedical Engineering Program, University of Arkansas, Fayetteville, AR, USA
2 Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: mkavdia{at}uark.edu.
Venular endothelial cells can release nitric oxide (NO) in response to intraluminal flow both in isolated venules and in vivo. Experimental studies suggest that venular endothelium-released nitric oxide causes dilation of the adjacent paired arteriole. In the vascular wall NO stimulates its target hemoprotein soluble guanylate cyclase (sGC) that relaxes smooth muscle cells. In this study, a computational model of NO transport for an arteriole and venule pair is developed to determine the importance of the venular endothelium-released nitric oxide and its transport to adjacent arteriole in the tissue. The model predicts that the tissue NO levels are affected within a wide range of parameters including NO-RBC reaction rate and NO production rate in arteriole and venule. The results predict that changes in the venular NO production not only affected venular endothelial and smooth muscle NO concentration, but also endothelial and smooth muscle NO concentration in the adjacent arteriole. This suggests that the anatomy of microvascular tissue can permit the transport of NO from arteriolar to venular side and vice versa and may provide a mechanism for dilation of proximal arterioles by venules. These results will have significant implications for our understanding of tissue NO levels in both physiological and pathophysiological conditions.
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