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Am J Physiol Heart Circ Physiol (February 18, 2005). doi:10.1152/ajpheart.00923.2003
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Submitted on September 29, 2003
Accepted on February 16, 2005

{alpha}v{beta}3 and {alpha}5{beta}1 Integrin Blockade Inhibit Myogenic Constriction of Skeletal Muscle Resistance Arterioles

Luis A Martinez-Lemus1, Tracy Crow1, Michael J Davis1, and Gerald A Meininger1*

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

* To whom correspondence should be addressed. E-mail: gam{at}tamu.edu.

In isolated resistance arterioles with spontaneous tone, ligation of {alpha}4{beta}1 and {alpha}5{beta}1 integrins induces vasoconstriction while ligation of {alpha}v{beta}3 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 integrins {alpha}4{beta}1, {alpha}5{beta}1, and {alpha}v{beta}3 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), the {alpha}4{beta}1 binding peptide (LDV), or an anti-{alpha}4 antibody. In contrast, {alpha}5{beta}1 integrin blockade with either anti-{alpha}5 or anti-{beta}1 caused a significant inhibition of myogenic constriction. Also, both RGD peptide and anti-{beta}3 antibody inhibited myogenic constriction. These results indicate that {alpha}5{beta}1 and {alpha}v{beta}3 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.




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