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1 Department of Physiology and Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and 2 Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas 75235
This study examined the response to
nitric oxide (NO) in rat middle cerebral arteries (MCA). NO donors
increased the activity of a 205-pS K+ channel recorded from
vascular smooth muscle (VSM) cells isolated from MCA 10-fold. Blockade
of guanylyl cyclase activity with
1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ, 10
5 M) did not alter the effect of NO on this
channel. In contrast, adding 20-hydroxyeicosatetraenoic acid (20-HETE)
to the bath (107 M) abolished the response to NO. NO
donors also increased the diameter of serotonin-preconstricted MCA to
85% of control. Blockade of K+ channels with iberiotoxin
or a high-K+ medium reduced this response by 50%. ODQ
(105 M) reduced this response by 47 ± 3%, whereas
preventing the fall of 20-HETE levels reduced the response by 59 ± 2% (n = 5). Blockade of both pathways eliminated
the response to NO donors. These results indicate that activation of
K+ channels contributes 50% to vasodilator response to NO
in rat MCA. This is mediated by a fall in 20-HETE levels rather than a
rise in cGMP levels or a direct effect of NO.
vascular smooth muscle; cytochrome P-450; potassium ion channels; cerebral circulation; 20-hydroxyeicosatetraenoic acid
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