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Articles in PresS, published online ahead of print January 10, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00699.2001
Submitted on August 6, 2001
Accepted on January 3, 2002
1 Physiology and Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: rroman{at}mcw.edu.
This study examined the mechanism by which cGMP contributes to the vasodilator response to NO in rat middle cerebral arteries (MCA). Administration of a NO donor, DEA-NONOate, or 8-Br-cGMP increased the diameter of serotonin preconstricted MCA by 79±3%. The response to DEA-NONOate, but not 8-Br-cGMP, was attenuated by iberiotoxin (10-7 M) or a 80 mM high K+ media, suggesting that activation of K+ channels contributes to the vasodilator response to NO, but not 8-Br-cGMP. The effects of NO and cGMP on the vasoconstrictor response to Ca2+ were also studied in MCA that were permeabilized with a-toxin and ionomycin. Elevations in bath Ca2+, from 10-8 to 10-5 M, decreased the diameter of permeabilized MCA by 76±5%. DEA-NONOate (10-6 M) and 8-Br-cGMP (10-4 M) blunted this response by 60%. Inhibition of guanylyl cyclase with 1H-[1,2,4] oxadiazole [4,3-a] quinoxalin-1-one (ODQ, 10-5 M) blocked the inhibitory effect of the NO donor, but not 8-Br-cGMP, on Ca2+-induced vasoconstriction. 8-Br-cGMP (10-4 M) had no effect on intracellular calcium concentration in control, serotonin-stimulated or 
-toxin and ionomycin permeabilized VSM cells isolated from the MCA. These results indicate that the vasodilator response to NO in rat MCA is mediated by activation of KCa channels via a cGMP-independent pathway and that cGMP also contributes to the vasodilator response to NO by decreasing the contractile response to elevations in intracellular calcium concentration.
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