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Department of Physiology, Monash University, Melbourne, Victoria 3800, Australia
Glycyrrhetinic acid (GA)
derivatives have been used to implicate gap junctions in vasorelaxation
attributed to endothelium-derived hyperpolarizing factor (EDHF). The
aim of this study was to assess whether GA compounds affect endothelial
cell hyperpolarization. Membrane potentials were recorded from
dye-identified endothelial and smooth muscle cells of guinea pig
coronary and rat mesenteric arteries. GA derivatives had varied effects
on the resting membrane potential: depolarization, hyperpolarization,
or no effect, depending on the artery. 18
-GA (50 µM) had a small
variable effect on ACh-induced hyperpolarizations in endothelial cells.
18
-GA (30 µM) and carbenoxolone (100 µM) significantly reduced
ACh-induced hyperpolarizations in both endothelial and smooth muscle
cells. Smooth muscle action potentials in rat tail arteries were
smaller and slower in the presence of 18-GA. Nerve-induced
excitatory junction potentials were inhibited by 18-GA and
carbenoxolone, whereas the time course of their decay initially
increased and then decreased. In conclusion, the GA compounds had a
range of effects. Their inhibition of the EDHF hyperpolarization and
relaxation in the smooth muscle may stem from the inhibition of
endothelial cell hyperpolarization.
gap junctions; glycyrrhetinic acid; action potentials; carbenoxolone; endothelium-derived hyperpolarizing factor
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