On the role of mechanosensitive mechanisms eliciting reactive hyperemia

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Abstract
We hypothesized that changes in hemodynamic forces such as pressure (P) and flow (F) contribute importantly to the development of reactive hyperemia. To exclude the effects of vivo factors, isolated rat skeletal muscle arterioles (∼130 μm) were utilized. We found that changes in P or P + F following occlusions elicited reactive dilations (RD). The peak of RD (up to ∼45 μm), but not the duration of RD, increased to changes in P (80 to 10, then back to 80 mmHg) as a function of the length of occlusions (30, 60, and 120 s). However, changes in P + F (80–10 -80 mmHg + 25–0-25 μl/min) increased both the peak and duration of RD (from ∼25 to 90 s) with longer occlusions. When only P changed, inhibition of nitric oxide synthesis or endothelium removal (E−) reduced only the peak of RD, whereas when P + F were changed, both the peak and duration of RD became reduced. Inhibition of stretch-activated cation channels by gadolinium reduced the peak but enhanced the duration of RD (both to P or P + F) that was unaffected by N G-nitro-l-arginine methyl ester (l-NAME) or by E−. When only P changed, inhibition of tyrosine kinases by genistein reduced peak RD but did not affect the RD duration. However, when P + F changed, genistein reduced both the peak and the duration of RD, additional l-NAME reduced the peak RD, but did not affect the duration of RD. Thus in isolated arterioles an RD resembling the characteristics of reactive hyperemia can be generated that is elicited by deformation, stretch, pressure, and flow/shear stress-sensitive mechanisms and is, in part, mediated by nitric oxide.