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This Article Full Text Full Text (PDF) All Versions of this Article: 291/2/H724    most recent 01215.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Kim, M.-h. Articles by Harris, N. R. Search for Related Content PubMed PubMed Citation Articles by Kim, M.-h. Articles by Harris, N. R.

Leukocyte adherence inhibits adenosine-dependent venular control of arteriolar diameter and nitric oxide

Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana

Submitted 16 November 2005 ; accepted in final form 23 March 2006

Venular control of arteriolar perfusion has been the focus of several investigations in recent years. This study investigated 1) whether endogenous adenosine helps control venule-dependent arteriolar dilation and 2) whether venular leukocyte adherence limits this response via an oxidant-dependent mechanism in which nitric oxide (NO) levels are decreased. Intravital microscopy was used to assess changes in arteriolar diameters and NO levels in rat mesentery. The average resting diameter of arterioles (27.5 ± 1.0 µm) paired with venules with minimal leukocyte adherence (2.1 ± 0.3 per 100-µm length) was significantly larger than that of unpaired arterioles (24.5 ± 0.8 µm) and arterioles (23.3 ± 1.3 µm) paired with venules with higher leukocyte adherence (9.0 ± 0.5 per 100-µm length). Local superfusion of adenosine deaminase (ADA) induced significant decreases in diameter and perivascular NO concentration in arterioles closely paired to venules with minimal leukocyte adherence. However, ADA had little effect on arterioles closely paired to venules with high leukocyte adherence or on unpaired arterioles. To determine whether the attenuated response to ADA for the high-adherence group was oxidant dependent, the responses were also observed in arterioles treated with 10^–4 M Tempol. In the high-adherence group, Tempol fully restored NO levels to those of the low-adherence group; however, the ADA-induced constriction remained attenuated, suggesting a possible role for an oxidant-independent vasoconstrictor released from the inflamed venules. These findings suggest that adenosine- and venule-dependent dilation of paired arterioles may be mediated, in part, by NO and inhibited by venular leukocyte adherence.

leukocyte adhesion; Tempol

This article has been cited by other articles:

				M.-h. Kim, P. R. Carter, and N. R. Harris P-selectin-mediated adhesion impairs endothelium-dependent arteriolar dilation in hypercholesterolemic mice Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H632 - H638. [Abstract] [Full Text] [PDF]