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Impaired flow-induced dilation in mesenteric resistance arteries from receptor protein tyrosine phosphatase-µ-deficient mice

¹Department of Medical Oncology and ²Department of Haematology, University Medical Centre Utrecht, Utrecht; ³Department of Pharmacology and Pharmacotherapy and ⁴Department of Medical Physics, Academic Medical Center Amsterdam, Amsterdam, The Netherlands; and ⁵Department of Biology, University of Scranton, Scranton, Pennsylvania

Submitted 28 May 2004 ; accepted in final form 5 November 2004

The transmembrane receptor-like protein tyrosine phosphatase-µ (RPTPµ) is thought to play an important role in cell-cell adhesion-mediated processes. We recently showed that RPTPµ is predominantly expressed in the endothelium of arteries and not in veins. Its involvement in the regulation of endothelial adherens junctions and its specific arterial expression suggest that RPTPµ plays a role in controlling arterial endothelial cell function and vascular tone. To test this hypothesis, we analyzed myogenic responsiveness, flow-induced dilation, and functional integrity of mesenteric resistance arteries from RPTPµ-deficient (RPTPµ^–/–) mice and from wild-type littermates. Here, we show that cannulated mesenteric arteries from RPTPµ^–/– mice display significantly decreased flow-induced dilation. In contrast, mechanical properties, myogenic responsiveness, responsiveness to the vasoconstrictors phenylephrine or U-46619, and responsiveness to the endothelium-dependent vasodilators methacholine or bradykinin were similar in both groups. Our results imply that RPTPµ is involved in the mechanotransduction or accessory signaling pathways that control shear stress responses in mesenteric resistance arteries.

endothelium; shear stress; protein phosphatase; transgenic mice; mechanotransduction

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