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

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.