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Integrins mediate mechanical compression-induced endothelium-dependent vasodilation through endothelial nitric oxide pathway.

Lu X, Kassab GS - J. Gen. Physiol. (2015)

Bottom Line: We cannulated isolated swine (n = 39) myocardial (n = 69) and skeletal muscle (n = 60) arteriole segments and exposed them to cyclic transmural pressure generated by either intraluminal or extraluminal pressure pulses to simulate compression in contracting muscle.It was attenuated by inhibition of NO synthase and by mechanical removal of the endothelium.We therefore conclude that integrin plays a role in cyclic compression-induced endothelial NO production and thereby in the vasodilation of small arteries during cyclic transmural pressure loading.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biomedical Engineering, Department of Cellular and Integrative Physiology, Department of Surgery, and Indiana Center for Vascular Biology and Medicine, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202.

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Endothelial role in the cyclic transmural pressure–induced vasodilation. The cyclic transmural pressure induced the vasodilation in precontracted coronary and skeletal muscular small arterial segments, and the vasodilation was inhibited by nonselective NOS inhibitor or denuded endothelium. (A) Cyclic transmural pressure–induced vasodilation persisted for at least 20 min. (B) Administration of L-NAME caused a dynamic vasoconstriction during cyclic transmural pressure. SNP, sodium nitroprusside (a NO donor). (C) Cyclic transmural pressure–induced vasodilation was inhibited by the mechanical removal of endothelium by a vessel diameter–matched wire.
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fig3: Endothelial role in the cyclic transmural pressure–induced vasodilation. The cyclic transmural pressure induced the vasodilation in precontracted coronary and skeletal muscular small arterial segments, and the vasodilation was inhibited by nonselective NOS inhibitor or denuded endothelium. (A) Cyclic transmural pressure–induced vasodilation persisted for at least 20 min. (B) Administration of L-NAME caused a dynamic vasoconstriction during cyclic transmural pressure. SNP, sodium nitroprusside (a NO donor). (C) Cyclic transmural pressure–induced vasodilation was inhibited by the mechanical removal of endothelium by a vessel diameter–matched wire.

Mentions: After a transient change of the vasodilation for ∼20 min, we verified that L-NAME was sufficient to inhibit the cyclic transmural pressure–induced endothelium-dependent vasodilation. Fig. 3 A shows a dynamic vasodilation for 20 min induced by cyclic transmural pressure. Fig. 3 B shows that the cyclic transmural pressure–induced vasodilation was gradually attenuated by L-NAME administration; i.e., L-NAME gradually replaced l-arginine, which is the substrate for eNOS to produce NO. The agonist-induced endothelium-dependent or -independent vasodilation was also verified after cyclic transmural pressure by use of BK, ACh, or SNP. The observations suggest that NO mediates cyclic transmural pressure–induced vasodilation. Because L-NAME also inhibits iNOS and nNOS (Pou et al., 1992; Haul et al., 1999), we further determined that the cyclic transmural pressure–induced vasodilation was eliminated after the endothelium was mechanically denuded by a diameter-matched wire (Fig. 3 C); i.e., endothelial NO mediates the cyclic transmural pressure–induced vasodilation.


Integrins mediate mechanical compression-induced endothelium-dependent vasodilation through endothelial nitric oxide pathway.

Lu X, Kassab GS - J. Gen. Physiol. (2015)

Endothelial role in the cyclic transmural pressure–induced vasodilation. The cyclic transmural pressure induced the vasodilation in precontracted coronary and skeletal muscular small arterial segments, and the vasodilation was inhibited by nonselective NOS inhibitor or denuded endothelium. (A) Cyclic transmural pressure–induced vasodilation persisted for at least 20 min. (B) Administration of L-NAME caused a dynamic vasoconstriction during cyclic transmural pressure. SNP, sodium nitroprusside (a NO donor). (C) Cyclic transmural pressure–induced vasodilation was inhibited by the mechanical removal of endothelium by a vessel diameter–matched wire.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4555471&req=5

fig3: Endothelial role in the cyclic transmural pressure–induced vasodilation. The cyclic transmural pressure induced the vasodilation in precontracted coronary and skeletal muscular small arterial segments, and the vasodilation was inhibited by nonselective NOS inhibitor or denuded endothelium. (A) Cyclic transmural pressure–induced vasodilation persisted for at least 20 min. (B) Administration of L-NAME caused a dynamic vasoconstriction during cyclic transmural pressure. SNP, sodium nitroprusside (a NO donor). (C) Cyclic transmural pressure–induced vasodilation was inhibited by the mechanical removal of endothelium by a vessel diameter–matched wire.
Mentions: After a transient change of the vasodilation for ∼20 min, we verified that L-NAME was sufficient to inhibit the cyclic transmural pressure–induced endothelium-dependent vasodilation. Fig. 3 A shows a dynamic vasodilation for 20 min induced by cyclic transmural pressure. Fig. 3 B shows that the cyclic transmural pressure–induced vasodilation was gradually attenuated by L-NAME administration; i.e., L-NAME gradually replaced l-arginine, which is the substrate for eNOS to produce NO. The agonist-induced endothelium-dependent or -independent vasodilation was also verified after cyclic transmural pressure by use of BK, ACh, or SNP. The observations suggest that NO mediates cyclic transmural pressure–induced vasodilation. Because L-NAME also inhibits iNOS and nNOS (Pou et al., 1992; Haul et al., 1999), we further determined that the cyclic transmural pressure–induced vasodilation was eliminated after the endothelium was mechanically denuded by a diameter-matched wire (Fig. 3 C); i.e., endothelial NO mediates the cyclic transmural pressure–induced vasodilation.

Bottom Line: We cannulated isolated swine (n = 39) myocardial (n = 69) and skeletal muscle (n = 60) arteriole segments and exposed them to cyclic transmural pressure generated by either intraluminal or extraluminal pressure pulses to simulate compression in contracting muscle.It was attenuated by inhibition of NO synthase and by mechanical removal of the endothelium.We therefore conclude that integrin plays a role in cyclic compression-induced endothelial NO production and thereby in the vasodilation of small arteries during cyclic transmural pressure loading.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biomedical Engineering, Department of Cellular and Integrative Physiology, Department of Surgery, and Indiana Center for Vascular Biology and Medicine, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202.

Show MeSH
Related in: MedlinePlus