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Department of Pathophysiology, Semmelweis University, 1445-Budapest, Hungary; and Department of Physiology, New York Medical College, Valhalla, New York 10595
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
NG-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.
isolated arteriole; stretch; pressure; flow; endothelium; nitric oxide; tyrosine kinase
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