Y. Saito et al., ROLE OF VENULAR ENDOTHELIUM IN CONTROL OF ARTERIOLAR DIAMETER DURING FUNCTIONAL HYPEREMIA, The American journal of physiology, 267(3), 1994, pp. 80001227-80001231
This study was designed to determine the importance of the venular end
othelium in the vasodilation of adjacent arterioles during functional
hyperemia. The hamster cremaster muscle was prepared for in vivo micro
scopy. Two silver-silver chloride electrodes were placed across the pe
dicle of the cremaster muscle, and a square-wave pulse (10 V amplitude
, 1 ms duration, and 1 Hz frequency) was used to elicit muscle contrac
tion. Muscle stimulation for 1 min resulted in a vasodilation of the f
irst-order arterioles from 74 +/- 2 to 91 +/- 2 mu m (n = 9, P < 0.05)
. After perfusion of the venule with air to disrupt the venular endoth
elium, there was no significant effect on the resting diameter, 73 +/-
3 mu m, but the vasodilation associated with the muscle stimulation w
as significantly attenuated to 82 +/- 3 mu m (P < 0.01). After complet
ion of these experiments, the disruption of venular endothelium was co
nfirmed by electron microscopy. The functional vasodilation of arterio
les adjacent to venules with an intact endothelium (venules in which a
ir did not enter) was retained after air perfusion (n = 6). These resu
lts suggest that the presence of the venular endothelium is important
for the arteriolar vasodilation during functional hyperemia. We propos
e that the venular endothelium releases a relaxing factor responsible
for a portion of the functional arteriolar vasodilation.