RGD Reference Report - Substance P is involved in the cutaneous blood flow increase response to sympathetic nerve stimulation in persistently inflamed rats. - Rat Genome Database

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Substance P is involved in the cutaneous blood flow increase response to sympathetic nerve stimulation in persistently inflamed rats.

Authors: Koeda, T  Tamura, R  Sato, J  Mizumura, K 
Citation: Koeda T, etal., J Physiol Sci. 2007 Dec;57(6):361-6. Epub 2007 Dec 4.
RGD ID: 2304327
Pubmed: PMID:18053315   (View Abstract at PubMed)
DOI: DOI:10.2170/physiolsci.RP007607   (Journal Full-text)

Changed vascular functions have been reported in several pathological conditions, such as chronic regional pain syndrome, obstructive vascular disease, and inflammation. Our previous experiments also showed that electrical stimulation of the lumbar sympathetic trunk (sympathetic stimulation: SS), which normally induces a decrease in blood flow (BF), caused a BF increase in about half of the measured sites in rats persistently inflamed with complete Freund's Adjuvant (AI rats). We also showed that the BF-increase response was only partially suppressed by the alpha1 antagonist at a higher dosage, suggesting the involvement of nonadrenergic mechanisms. We hypothesize that nonadrenergic mechanisms mediating vasodilatation might involve a vasodilating neuropeptide such as substance P (SP) that is released from sympathetic nerve terminals. In this experiment, we conducted an examination using an NK-1 receptor antagonist to determine whether SP plays any role in changed response to SS in AI rats, and also an immunohistochemical examination of whether SP is expressed in the lumbar sympathetic nerve ganglia (SG) of AI rats. The administration of an NK-1 receptor antagonist, CP-96,345, significantly reduced the BF-increase response to SS in AI rats, but its inactive enantiomer, CP-96,344, had no effect. Immunohistochemistry for SP revealed that SP-ir positive SG neurons (mean 13 neurons/rat) were found in 5 of 8 AI rats, whereas only one neuron was stained in 8 control rats. These results suggest that NK-1 receptor activation is involved in the BF-increase response to SS, and that this activation is in part mediated by SP from lumbar SG that was synthesized de novo in inflamed animals.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Inflammation  ISOTac1 (Rattus norvegicus)2304327; 2304327protein:increased expression:neuronRGD 
Inflammation  ISOTacr1 (Rattus norvegicus)2304327; 2304327 RGD 
Inflammation  IEP 2304327protein:increased expression:neuronRGD 
Inflammation  IMP 2304327 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tac1  (tachykinin, precursor 1)
Tacr1  (tachykinin receptor 1)

Genes (Mus musculus)
Tac1  (tachykinin 1)
Tacr1  (tachykinin receptor 1)

Genes (Homo sapiens)
TAC1  (tachykinin precursor 1)
TACR1  (tachykinin receptor 1)


Additional Information