M. Szentivanyi et al., VENOUS MYOGENIC TONE AND ITS REGULATION THROUGH K+ CHANNELS DEPENDS ON CHRONIC INTRAVASCULAR PRESSURE, Circulation research, 81(6), 1997, pp. 988-995
In this study, we compared the level of myogenic tone and its negative
-feedback control through specific K+ channels in two types of human v
eins (saphenous [SV] and cephalic [CV] veins), which experience differ
ent ranges of pressure in vivo. We also investigated whether an experi
mental model of increased venous pressure in rats exposed to head-up t
ilt for 2 weeks produced changes similar to those observed in the huma
n veins. Cylindrical vein segments were cannulated, their diameters we
re measured, and the intraluminal pressure was set at different levels
(2 to 30 mm Hg) in vitro. Acetylcholine test showed that during the r
egular harvesting process 76% of the human SVs exposed for coronary by
pass grafts had no functional endothelium. We found significant myogen
ic tone in the human SV, where the in vivo pressure is high, but it wa
s not present in the human CV, where the in vivo pressure is low. The
nonspecific K+ channel antagonist, tetraethylammonium (TEA), decreased
the diameter of the human SV but not the CV. Iberiotoxin and 4-aminop
yridine, blockers of the Ca2+-sensitive (K-Ch) and voltage-gated K+ (K
-V) channels, also decreased the diameter of the human SV by 10.2+/-4.
8% and 19.5+/-4.7%, respectively. In the rat SV, significant myogenic
tone was found, but TEA had no effect, even after 2 weeks of in vivo p
ressure increase in the hindlimb by head-up tilt. We conclude that (1)
an increased venous myogenic tone correlates with higher chronic intr
aluminal pressure loads, (2) K-Ca and K-V channels counterregulate the
myogenic tone in human, but not in rat, saphenous vein, (3) the count
erregulatory effect is more effective at high than at low intraluminal
in vitro pressure levels, and (4) its development is probably a long-
term process.