Background-Physical forces, such as pressure and flow, are well known to af
fect vascular function in the coronary circulation. Increases in shear stre
ss produce vasodilation in coronary arterioles in vitro, and constant-flow
preparations suggest a role for sheer stress-induced vasodilation during ad
justments to metabolic demand in vivo. Hypothetically, the regulation of sh
ear stress can be viewed as a negative feedback control scheme (increased v
elocity --> increased shear --> vasodilation --> decreased velocity --> she
ar normalized). Therefore, we hypothesized that shear stress would be at le
ast partially regulated during conditions of elevated flow.
Methods and Results-We used fluorescence microangiography to measure microv
ascular diameters and velocities in the coronary circulation in vivo and us
ed these variables to calculate shear stress. Measurements were obtained un
der basal conditions, during maximal coronary blood flow, and after inhibit
ion of NO synthase. Basal shear stress in the coronary circulation averaged
10 dyn/cm(2) in small arteries and 19 dyn/cm(2) in arterioles. Regulation
of shear stress was observed in small arteries during adenosine-induced inc
reases in coronary blood flow, but arterioles showed minimal regulation. NO
synthase blockade had no effect on basal shear stress but completely aboli
shed its regulation in small arteries during vasodilation.
Conclusions-Our data provide the first quantitative estimates of microvascu
lar shear stress in the coronary circulation. Moreover, our results suggest
that shear stress in small coronary arteries is regulated by NO release fr
om the endothelium.