6533b853fe1ef96bd12acd3a
RESEARCH PRODUCT
Nitric oxide modulates cerebral blood flow stimulation by acetazolamide in the rat cortex: a laser Doppler scanning study
J TuettenbergAxel HeimannOliver Kempskisubject
MaleArginineVasodilator AgentsHemodynamicsBlood PressureStimulationPharmacologyNitric OxideNitroarginineNitric oxidechemistry.chemical_compoundLaser-Doppler FlowmetrymedicineAnimalsNitric Oxide DonorsRats WistarCarbonic Anhydrase InhibitorsCerebral CortexChemistryGeneral NeuroscienceLaser Doppler velocimetryRatsAcetazolamidemedicine.anatomical_structurenervous systemCerebral blood flowCerebral cortexCerebrovascular CirculationMolsidomineAnesthesiaNitric Oxide SynthaseAcetazolamidecirculatory and respiratory physiologymedicine.drugdescription
Abstract The involvement of nitric oxide (NO) in cerebral blood flow (CBF) stimulation by acetazolamide was studied in anaesthetised, mechanically ventilated Wistar rats. CBF was monitored by laser Doppler scanning. Acetazolamide induced a long-lasting significant rCBF-increase. Application of N G -Nitro- l -arginine (L-NNA), an inhibitor of all NO synthetases (NOS), prevented CBF stimulation by acetazolamide. Continuous infusion of the exogenous NO donor SIN-1 (3-morpholinosydnonimine) suppressed L-NNA induced increases of mean arterial blood pressure without effect on rCBF in comparison to baseline. Additional acetazolamide injection then again caused a significant increase of rCBF in spite of NOS-inhibition. We thus conclude that NO is involved in acetazolamide-induced CBF stimulation. The mere continuous presence of NO is sufficient to re-establish the acetazolamide-response in spite of NOS-inhibition. These data suggest that NO acts rather as a modulator than as a mediator of the acetazolamide-induced CBF response.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2001-11-01 | Neuroscience Letters |