In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 277, No. 2 ( 1999-08-01), p. H799-H811
Abstract:
We investigated the role of nitric oxide (NO)/cGMP in the coupling of neuronal activation to regional cerebral blood flow (rCBF) in α-chloralose-anesthetized rats. Whisker deflection (60 s) increased rCBF by 18 ± 3%. NO synthase (NOS) inhibition by N ω -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 andl-NNA-induced attenuation of the whisker response in the presence ofl-NNA, whereas the NO-independent vasodilator papaverine (1 mM) had no effect on the whisker response. Basal cGMP levels were decreased to 35% byl-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 1 H-[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.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.1999.277.2.H799
Language:
English
Publisher:
American Physiological Society
Publication Date:
1999
detail.hit.zdb_id:
1477308-9
SSG:
12
Permalink