Magnitude of upregulated dilation to l-arginine is related to arteriolar shear rate upstream

We have shown that the wall shear stress is significantly higher and more variable upstream (vs. downstream) along a transverse artenole (diam. μ25μm) (AJP 265:H1682-H1687,1993). We have recently shown that a conducted signal initiated by L-arginine downstream both induces a conducted vasodilation upstream and upregulates the ability of the upstream region of the transverse arteriole to dilate to locally applied L-arginine (Circ. Res. 77:695-701,1995). Our purpose here was to determine whether the magnitude of the upregulated dBation to L-arginine was related to the fluid shearing forces in the upstream region of the transverse arteriole. Arteriolar diameter and red blood cell velocities (XRITC labeled cells) were obtained for sequential branch points along a transverse arteriole in anesthetized (Nembutal 70mg/kg) Golden hamsters (N=5). The baseline shear rate ranged between 161 and 3278 sec^-1 (916±223 sec^-1; mean±SEM; n=10) upstream, and between 180 and 562 sec^-1 (323±23 sec^-1, n=5) downstream. We have previously reported the upregulated dilation to L-arginine in these animals (range: 7 to 170% increase in diameter compared to baseline) (Circ. Res. 77:695-701,1995). Here we report that the upregulated dilation was greater when the basefcie shear rate upstream was greater (r=0.80 for shear rate in the upstream feed; and r=0.76 for shear rate h Ine upstream branches). However, the upregulated dilation upstream (which is upregulated only after downstream exposure to L-arginine) was unrelated to the shear rate ii the downstream portion of the feed (r=0.46) or branches (r=0.35). Our data suggest that the shearing forces in the upstream region of these arterioles modulates the upregulated dtation to L-arghne.