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Am J Physiol Heart Circ Physiol 277: H799-H811, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 2, H799-H811, August 1999

Nitric oxide: a modulator, but not a mediator, of neurovascular coupling in rat somatosensory cortex

Ute Lindauer, Dirk Megow, Hiroshi Matsuda, and Ulrich Dirnagl

Department of Experimental Neurology, Humboldt University, Charité Hospital, 10098 Berlin, Germany

We investigated the role of nitric oxide (NO)/cGMP in the coupling of neuronal activation to regional cerebral blood flow (rCBF) in alpha -chloralose-anesthetized rats. Whisker deflection (60 s) increased rCBF by 18 ± 3%. NO synthase (NOS) inhibition by Nomega -nitro-L-arginine (L-NNA; topically) reduced the rCBF response to 9 ± 4% and resting rCBF to 80 ± 8%. NO donors [S-nitroso-N-acetylpenicillamine (SNAP; 50 µM), 3-morpholinosydnonimine (10 µM)] or 8-bromoguanosine 3',5'-cyclic-monophosphate (8-BrcGMP; 100 µM)] restored resting rCBF and L-NNA-induced attenuation of the whisker response in the presence of L-NNA, whereas the NO-independent vasodilator papaverine (1 mM) had no effect on the whisker response. Basal cGMP levels were decreased to 35% by L-NNA and restored to 65% of control by subsequent SNAP superfusion. Inhibition of neuronal NOS by 7-nitroindazole (7-NI; 40 mg/kg ip) or soluble guanylyl cyclase by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 100 µM) significantly reduced resting rCBF to 86 ± 8 and 92 ± 10% and whisker rCBF response to 7 ± 4 and 12 ± 3%, respectively. ODQ reduced tissue cGMP to 54%. 8-BrcGMP restored the whisker response in the presence of 7-NI or ODQ. We conclude that NO, produced by neuronal NOS, is a modulator in the coupling of neuronal activation and rCBF in rat somatosensory cortex and that this effect is mainly mediated by cGMP. L-NNA-induced vasomotion was significantly reduced during increased neuronal activity and after restoration of basal NO levels, but not after restoration of cGMP.

whisker stimulation; laser Doppler flowmetry; cerebral circulation; nitric oxide synthase inhibition; guanylyl cyclase; vasomotion


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