Jl. Jasperse et Mh. Laughlin, FLOW-INDUCED DILATION OF RAT SOLEUS FEED ARTERIES, American journal of physiology. Heart and circulatory physiology, 42(5), 1997, pp. 2423-2427
Flow-induced dilation is thought to contribute to dilation of skeletal
muscle arteries and arterioles during exercise hyperemia. We sought t
o determine whether rat soleus feed arteries (SFA) exhibit flow-induce
d dilation and to evaluate the potential contribution of flow-induced
dilation of SFA to exercise hyperemia. Rat SFA were isolated and cannu
lated to allow pressure and intraluminal flow to be independently cont
rolled. Intraluminal pressure was maintained at 90 cmH(2)O throughout
the experiment. All SFA (n = 13) developed spontaneous tone and dilate
d in response to flow. Flow of 10 and 14 mu l/min produced a 34 +/- 14
and 56 +/- 17 mu m increase above basal diameter (135 +/- 12 mu m), r
espectively. Flows >14 mu l/min produced little further dilation. Maxi
mum flow-induced dilation was 86 +/- 3% of passive diameter determined
in calcium-free physiological saline solution. Calculated shear stres
s was maintained at 4-6 dyn/cm(2) at flows of 10-20 mu l/min but incre
ased at greater flows because SFA did not dilate further. To determine
whether dilation in response to flows in this range may contribute to
exercise hyperemia, we estimated in vivo SFA blood flows from previou
sly published soleus blood flow data. Anesthetized rats are estimated
to have hows of 10 mu l/min per SFA, and conscious rats are estimated
to have flows of 95 (nonexercising), 153 (walking), and 225 (running)
mu l/min per SFA. Corresponding shear stresses were estimated to be 26
(anesthetized), 47 (conscious, nonexercising), 75 (walking), and 111
(running) dyn/cm(2). Because estimated in vivo values for both flow an
d wall shear stress are far greater than the flow and/or shear stresse
s at which maximal flow-induced dilation occurs in vitro, we conclude
that flow-induced dilation contributes little to dilation of SFA durin
g locomotory exercise.