RGD Reference Report - TRPV1-mediated protection against endotoxin-induced hypotension and mortality in rats. - Rat Genome Database

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TRPV1-mediated protection against endotoxin-induced hypotension and mortality in rats.

Authors: Wang, Y  Novotny, M  Quaiserova-Mocko, V  Swain, GM  Wang, DH 
Citation: Wang Y, etal., Am J Physiol Regul Integr Comp Physiol. 2008 May;294(5):R1517-23. Epub 2008 Mar 12.
RGD ID: 2304320
Pubmed: PMID:18337316   (View Abstract at PubMed)
PMCID: PMC2668825   (View Article at PubMed Central)
DOI: DOI:10.1152/ajpregu.00005.2008   (Journal Full-text)

This study was designed to test the hypothesis that the transient receptor potential vanilloid type 1 (TRPV1) channel, expressed primarily in sensory nerves, and substance P (SP), released by sensory nerves, play a protective role against lipopolysaccharide (LPS)-induced hypotension. LPS (10 mg/kg iv) elicited tachycardia and hypotension in anesthetized male Wistar rats, which peaked at 10 min and gradually recovered 1 h after the injection. Blockade of TRPV1 with its selective antagonist capsazepine (CAPZ, 3 mg/kg iv) impaired recovery given that the fall in mean arterial pressure (MAP) was greater 1 h after CAPZ plus LPS injections compared with LPS injection alone (45 +/- 5 vs. 25 +/- 4 mmHg, P < 0.05). Blockade of the neurokinin 1 (NK1) receptor with its selective antagonists RP-67580 (5 mg/kg iv) or L-733,060 (4 mg/kg iv) prevented recovery, considering that falls in MAP were not different 1 h after injections of NK1 antagonists plus LPS from their peak decreases (66 +/- 9 vs. 74 +/- 5 mmHg or 60 +/- 7 vs. 69 +/- 3 mmHg, respectively, P > 0.05). LPS increased plasma SP, norepinephrine (NE), and epinephrine (Epi) levels compared with vehicles, and the increases in plasma SP, NE, and Epi were significantly inhibited by CAPZ or RP-67580. The survival rate at 24 or 48 h after LPS injection (20 mg/kg ip) was lower in conscious rats pretreated with CAPZ or RP-67580 compared with rats treated with LPS alone (P < 0.05). Thus our results show that the TRPV1, possibly via triggering release of SP which activates the NK1 and stimulates the sympathetic axis, plays a protective role against endotoxin-induced hypotension and mortality, suggesting that TRPV1 receptors are essential in protecting vital organ perfusion and survival during the endotoxic condition.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Hypotension  ISOTac1 (Rattus norvegicus)2304320; 2304320 RGD 
Hypotension  ISOTacr1 (Rattus norvegicus)2304320; 2304320 RGD 
Hypotension  IMP 2304320; 2304320 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of blood pressure  IMP 2304320 RGD 
response to lipopolysaccharide  IEP 2304320 RGD 

Cellular Component
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
extracellular space  IDA 2304320 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