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Departments of 1 Physiology, 2 Pharmacology, and 3 Pathology, New York Medical College, Valhalla, New York 10595; 4 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75235; and 5 Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan 48202
Vasodilation to increases in flow was
studied in isolated gracilis muscle arterioles of female endothelial
nitric oxide synthase (eNOS)-knockout (KO) and female wild-type (WT)
mice. Dilation to flow (0-10 µl/min) was similar in the two
groups, yet calculated wall shear stress was significantly greater in
arterioles of eNOS-KO than in arterioles of WT mice. Indomethacin,
which inhibited flow-induced dilation in vessels of WT mice by ~40%,
did not affect the responses of eNOS-KO mice, whereas miconazole and
6-(2-proparglyoxyphenyl)hexanoic acid (PPOH) abolished the responses.
Basal release of epoxyeicosatrienonic acids from arterioles was
inhibited by PPOH. Iberiotoxin eliminated flow-induced dilation in
arterioles of eNOS-KO mice but had no effect on arterioles of WT mice.
In WT mice, neither
N
-nitro-L-arginine methyl ester
nor miconazole alone affected flow-induced dilation. Combination of
both inhibitors inhibited the responses by ~50%.
1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one
(ODQ) alone inhibited flow-induced dilation by ~49%. ODQ + indomethacin eliminated the responses. Thus, in arterioles of female WT
mice, nitric oxide and prostaglandins mediate flow-induced dilation.
When eNOS is inhibited, endothelium-derived hyperpolarizing factor
substitutes for nitric oxide. In female eNOS-KO mice, metabolites of
cytochrome P-450, via activation of large-conductance
Ca2+-activated K+ channels of smooth muscle,
mediate entirely the arteriolar dilation to flow.
nitric oxide; prostaglandins; hyperpolarizing factor; cytochrome P-450 metabolites; potassium channels
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