RGD Reference Report - Central neuropeptide Y signaling ameliorates N(omega)-nitro-L-arginine methyl ester hypertension in the rat through a Y1 receptor mechanism. - Rat Genome Database

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Central neuropeptide Y signaling ameliorates N(omega)-nitro-L-arginine methyl ester hypertension in the rat through a Y1 receptor mechanism.

Authors: Michalkiewicz, M  Zhao, G  Jia, Z  Michalkiewicz, T  Racadio, MJ 
Citation: Michalkiewicz M, etal., Hypertension 2005 Apr;45(4):780-5. Epub 2005 Feb 7.
RGD ID: 1357410
Pubmed: PMID:15699473   (View Abstract at PubMed)
DOI: DOI:10.1161/01.HYP.0000153953.69799.f2   (Journal Full-text)

Neuropeptide Y is a potent inhibitory neurotransmitter expressed in the central neurons that control blood pressure. NO also serves as an inhibitory neurotransmitter, and its deficit causes sympathetic overactivity, which then contributes to hypertension. This study tested the hypothesis that neuropeptide Y functions as a central neurotransmitter to lower blood pressure, therefore its increased signaling ameliorates hypertension induced by NO deficiency. Conscious neuropeptide Y transgenic male rats, overexpressing the peptide under its natural promoter, and nontransgenic littermates (controls) were used in this study. Neuropeptide Y, Y1 receptor antagonist BIBP3226, or vehicle (saline) were administered continuously for 14 days into the cerebral lateral ventricle in unrestrained animals using osmotic pumps. Blood pressure was measured by radiotelemetry. Compared with control animals, transgenic overexpression of neuropeptide Y significantly ameliorated (by 9.7+/-1.5 mm Hg) NO deficiency hypertension (induced by administration of N(omega)-nitro-L-arginine methyl ester in the drinking water). This hypotensive effect of neuropeptide Y upregulation was associated with reduced proteinuria and cardiac hypertrophy and fibrosis. Central administration of neuropeptide Y in nontransgenic rats also reduced (by 10.2+/-1.6 mm Hg) the NO deficiency hypertension, whereas a neuropeptide Y1 receptor antagonist centrally administered in the transgenic subjects during NO deficiency hypertension completely attenuated the depressor effect of neuropeptide Y upregulation. Thus, acting at the level of the central nervous system distinctively via a Y1 receptor-mediated mechanism, endogenous neuropeptide Y exerted a potent antihypertensive function, and its enhanced signaling ameliorated NO deficiency hypertension.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
hypertension  ISONpy (Rattus norvegicus)1357410; 1357410 RGD 
hypertension  ISONpy1r (Rattus norvegicus)1357410; 1357410 RGD 
hypertension  IMP 1357410; 1357410 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of blood pressure  IMP 1357410 RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
decreased heart weight inducedIAGPcontrolled NG-nitroarginine methyl ester content drinking water1357410compared to wild-type littermateRGD 
thin ventricular wall inducedIAGPcontrolled NG-nitroarginine methyl ester content drinking water1357410compared to wild-type littermateRGD 
Objects Annotated

Genes (Rattus norvegicus)
Npy  (neuropeptide Y)
Npy1r  (neuropeptide Y receptor Y1)

Genes (Mus musculus)
Npy  (neuropeptide Y)
Npy1r  (neuropeptide Y receptor Y1)

Genes (Homo sapiens)
NPY  (neuropeptide Y)
NPY1R  (neuropeptide Y receptor Y1)

Strains
SD-Tg(Npy)400Mcwi  (NA)


Additional Information