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_v3- and ₅₁-integrin blockade inhibits myogenic constriction of skeletal muscle resistance arterioles

Department of Medical Physiology, Cardiovascular Research Institute, Division of Vascular Biology, Texas A&M University System Health Science Center, College Station, Texas

Submitted 29 September 2003 ; accepted in final form 16 February 2005

In isolated resistance arterioles with spontaneous tone, ligation of ₄₁- and ₅₁-integrins induces vasoconstriction whereas ligation of _v3-integrin induces vasodilation. However, whether integrins directly participate in myogenic constriction to pressure elevation is not known. To answer this question, isolated rat skeletal muscle arterioles were exposed to step increments in pressure in the absence or presence of peptides and function-blocking antibodies known to bind ₄₁-, ₅₁-, or _v3-integrins while vessel diameter was continually monitored. Myogenic constriction, as assessed by the ability of isolated arterioles to reduce their diameter in response to two consecutive increments in intraluminal pressure (90–110 and 110–130 cmH₂O), was not affected by treatment with any of the control peptides (RAD, LEV), a control antibody (anti-rat major histocompatibility complex), an ₄₁-integrin-binding peptide (LDV), or an anti-₄-integrin antibody. In contrast, ₅₁-integrin blockade with either anti-₅- or anti-₁-integrin antibody caused a significant inhibition of myogenic constriction. Also, both RGD peptide and anti-₃-integrin antibody inhibited myogenic constriction. These results indicate that ₅₁- and _v3-integrins are necessary for myogenic constriction and further suggest that integrins are part of the mechanosensory apparatus responsible for the ability of vascular smooth muscle cells to detect and/or respond to changes in intraluminal pressure.

mechanosensors; spontaneous tone; autoregulation; mechanotransduction; microcirculation

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