Attenuation of conducted vasodilatation in the skeletal muscle during hyperhomocysteinemia

Abstract

Conduction of vasodilatation (CVD) from distal resistance arterioles to the proximal arterioles and feeding arteries during metabolic demand is mediated by intercellular gap junctions in the vascular endothelium. The role of Hyperhomocysteinemia (HHcy) in musculoskeletal system during CVD is unclear. We hypothesize that during HHcy there is impaired CVD due to decreased expression of endothelial associated connexins and thus decreases tissue perfusion to the contracting skeletal muscles.MethodsCVD studies are performed in gluteus maximus muscle preparation of wild type (C57BL6/J) and CBS‐/+ (HHcy) mice using intravital microscopy. Expression of connexins and myostatin protein is studied by western blot and Immunohistochemistry methods.ResultsThere is decreased CVD and tissue perfusion in response to Acetylcholine in the CBS‐/+ mice compared to wild type controls assessed by intravital microscopy and Laser Doppler. There is decreased expression of connexins and increased myostatin expression in CBS‐/+ mice compared to wild type controls.ConclusionOur findings suggest that CVD in skeletal muscle is decreased during hyperhomocysteinemia due to decreased expression of gap junction connexins.Source of Research support: NIH