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1 Department of Cell Biology and Physiology and 2 Department of Neurosciences, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131-5218
Nitric
oxide (NO) synthase (NOS) inhibition with
N
-nitro-L-arginine
(L-NNA) produces L-NNA hypertensive rats (LHR),
which exhibit increased sensitivity to voltage-dependent
Ca2+ channel-mediated vasoconstriction. We hypothesized
that enhanced contractile responsiveness after NOS inhibition is
mediated by depolarization of membrane potential
(Em) through attenuated K+ channel
conductance. Em measurements demonstrated that
LHR vascular smooth muscle cells (VSMCs) are depolarized in open,
nonpressurized (
44.5 ± 1.0 mV in control vs. 36.8 ± 0.8 mV in LHR) and pressurized mesenteric artery segments (41.8 ± 1.0 mV in control vs. 32.6 ± 1.4 mV in LHR). Endothelium
removal or exogenous L-NNA depolarized control VSMCs but
not LHR VSMCs. Superfused L-arginine hyperpolarized VSMCs
from both the control and LHR groups and reversed
L-NNA-induced depolarization (44.5 ± 1.0 vs.
45.8 ± 2.1 mV). A Ca2+-activated K+
channel agonist, NS-1619 (10 µM), hyperpolarized both groups of
arteries to a similar extent (from 50.8 ± 1.0 to 62.5 ± 1.2 mV in control and from 43.7 ± 1.1 to 55.6 ± 1.2 mV
in LHR), although Em was still different in the
presence of NS-1619. In addition, superfused iberiotoxin (50 nM)
depolarized both groups similarly. Increasing the extracellular
K+ concentration from 1.2 to 45 mM depolarized
Em, as predicted by the Goldman-Hodgkin-Katz
equation. These data support the hypothesis that loss of NO activation
of K+ channels contributes to VSMC depolarization in
L-NNA-induced hypertension without a change in the number
of functional large conductance Ca2+-activated
K+ channels.
NS-1619; vascular smooth muscle cells; potassium channels; nitric oxide synthase
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