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1 Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada; 2 Institute for Smooth Muscle Biology, Department of Urology and Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461; and 3 Department of Pharmacology and Therapeutics, University of Florida, Gainesville, Florida 32610
The effects of two
structurally distinct inhibitors of gap junction communication were
studied by using three different forms of vasoconstriction in
pressurized rat middle cerebral arteries. The sensitivity of myogenic
tone (at 60 mmHg), vasopressin-induced tone (10 nM, at 20 mmHg), and
depolarizing solution-induced tone (80 mM K+, at 20 mmHg)
to inhibition by heptanol (1.0 µM to 3.0 mM) or 18
-glycyrrhetinic
acid (18-GA, 1.0 to 50 µM) were determined. Pressure-induced
myogenic tone was inhibited by heptanol (IC50 = 0.75 ± 0.09 mM) and 18-GA (~30 µM). Vasopressin-induced
vasoconstriction was also inhibited by heptanol (IC50 = 0.4 ± 0.3 mM) and 18-GA (>1 µM). Depolarizing
solution-induced vasoconstriction was less sensitive to inhibition by
heptanol compared to vasopressin (P < 0.01) or
pressure-induced constriction (P < 0.05). However, 18-GA did not inhibit depolarization-induced constriction. Sharp microelectrode experiments on isolated arteries revealed stable membrane potentials, with no detectable effect of heptanol (1 mM) or
18-GA (20-30 µM) on the average membrane potential at 20 mmHg. However, 
20% of impaled cells (5 of 28) exhibited
uncharacteristic oscillations in membrane potential after
pharmacological uncoupling. At 60 mmHg a 7- to 9-mV
hyperpolarization and corresponding vasodilation (50%) was
observed, and the frequency of membrane potential oscillations doubled
(9 of 23 cells). These data indicate that gap junctions play an
important role in the maintenance and modulation of membrane potential
and tone in cerebral resistance arteries.
heptanol; glycyrrhetinic acid; vascular smooth muscle; resistance arteries; vasopressin and depolarization
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