RGD Reference Report - Neuronal nitric oxide mediates cerebral vasodilatation during acute hypertension. - Rat Genome Database

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Neuronal nitric oxide mediates cerebral vasodilatation during acute hypertension.

Authors: Talman, WT  Nitschke Dragon, D 
Citation: Talman WT and Nitschke Dragon D, Brain Res. 2007 Mar 30;1139:126-32. Epub 2007 Jan 8.
RGD ID: 1642146
Pubmed: PMID:17291465   (View Abstract at PubMed)
PMCID: PMC1885240   (View Article at PubMed Central)
DOI: DOI:10.1016/j.brainres.2007.01.008   (Journal Full-text)

Parasympathetic nerves from the pterygopalatine ganglia provide nitroxidergic innervation to forebrain cerebral blood vessels. Disruption of that innervation attenuates cerebral vasodilatation seen during acute hypertension as does systemic administration of a non-selective nitric oxide synthase (NOS) inhibitor. Although such studies suggest that nitric oxide (NO) released from parasympathetic nerves participates in vasodilatation of cerebral vessels during hypertension, that hypothesis has not been tested with selective local inhibition of neuronal NOS (nNOS). We tested that hypothesis through these studies performed in anesthetized rats instrumented for continuous measurement of blood pressure, heart rate and pial arterial diameter through a cranial window. We sought to determine if the nNOS inhibitor propyl-L-arginine delivered directly to the outer surface of a pial artery would (1) attenuate changes in pial arterial diameter during acute hypertension and (2) block nNOS-mediated dilator effects of N-methyl-D-aspartate (NMDA) delivered into the window but (3) not block vasodilatation elicited by acetylcholine (ACh) and mediated by endothelial NOS dilator. Without the nNOS inhibitor arterial diameter abruptly increased 70+/-15% when mean arterial pressure (MAP) reached 183+/-3 mm Hg while with nNOS inhibition diameter increased only 13+/-10% (p<0.05) even when MAP reached 191+/-4 mm Hg (p>0.05). The nNOS inhibitor significantly attenuated vasodilatation induced by NMDA but not ACh delivered into the window. Thus, local nNOS inhibition attenuates breakthrough from autoregulation during hypertension as does complete interruption of the parasympathetic innervation of cerebral vessels. These findings further support the hypothesis that NO released from parasympathetic fibers contributes to cerebral vasodilatation during acute hypertension.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
vasodilation  IMP 1642146 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nos1  (nitric oxide synthase 1)


Additional Information