RGD Reference Report - Vascular arginase contributes to arteriolar endothelial dysfunction in a rat model of hemorrhagic shock. - Rat Genome Database

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Vascular arginase contributes to arteriolar endothelial dysfunction in a rat model of hemorrhagic shock.

Authors: Johnson, RA  Durante, W  Craig, T  Peyton, KJ  Myers, JG  Stewart, RM  Johnson, FK 
Citation: Johnson RA, etal., J Trauma. 2010 Aug;69(2):384-91.
RGD ID: 4143274
Pubmed: PMID:20699748   (View Abstract at PubMed)
DOI: DOI:10.1097/TA.0b013e3181e771a3   (Journal Full-text)

BACKGROUND: Hemorrhagic shock causes hypoperfusion of peripheral tissues and promotes endothelial dysfunction, which may lead to further tissue injury. Trauma increases extrahepatic activity of arginase, an enzyme which competes for l-arginine with nitric oxide synthase, and plays a key role in the development of endothelial dysfunction during aging, hypertension, and diabetes. However, the role of arginase in hemorrhage-induced endothelial dysfunction has not been studied. This study tests the hypothesis that arginase inhibition improves endothelial function after hemorrhage. METHODS: Male Sprague-Dawley rats were implanted with indwelling arterial catheters for blood pressure measurements and blood removal. Awake animals were subjected to a 45% fixed volume controlled hemorrhage and blood pressure was monitored. Unbled rats served as controls. Skeletal muscle arterioles were isolated 24 hours after hemorrhage and cannulated in a pressure myograph system. To study endothelial function, arterioles were exposed to constant midpoint, but altered endpoint pressures, to establish graded levels of luminal flow and internal diameter was measured. RESULTS: Hemorrhage lowered mean arterial pressure that spontaneously recovered to 78% and 88% of baseline in 2 hours and 20 hours, respectively. Vascular arginase II and blood glucose levels were elevated, whereas hemoglobin and insulin levels were decreased 24 hours after blood loss. In posthemorrhage arterioles, flow-induced dilation was abolished. Acute in vitro treatment with an inhibitor of arginase, N-hydroxy-nor-l-arginine, restored flow-induced dilation to unbled control levels. Similarly, the arginase and nitric oxide synthase substrate, l-arginine, but not the inactive isomer, d-arginine, restored flow-induced dilation. CONCLUSIONS: These results indicate that arginase contributes to endothelial dysfunction in resistance vessels after significant hemorrhage.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Hemorrhagic Shock  ISOArg2 (Rattus norvegicus)4143274; 4143274protein:increased expression:aorta (rat)RGD 
Hemorrhagic Shock  IEP 4143274protein:increased expression:aorta (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Arg2  (arginase 2)

Genes (Mus musculus)
Arg2  (arginase type II)

Genes (Homo sapiens)
ARG2  (arginase 2)


Additional Information