RGD Reference Report - Peripheral mechanisms of erectile dysfunction in a rat model of chronic cocaine use. - Rat Genome Database

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Peripheral mechanisms of erectile dysfunction in a rat model of chronic cocaine use.

Authors: Kendirci, M  Pradhan, L  Trost, L  Gur, S  Chandra, S  Agrawal, KC  Hellstrom, WJ 
Citation: Kendirci M, etal., Eur Urol. 2007 Aug;52(2):555-63. Epub 2007 Mar 20.
RGD ID: 2292142
Pubmed: PMID:17420087   (View Abstract at PubMed)
DOI: DOI:10.1016/j.eururo.2007.03.022   (Journal Full-text)

OBJECTIVE: To evaluate the peripheral mechanisms of erectile dysfunction (ED) in a rat model of triple-binge cocaine administration. METHODS: Adult male Sprague-Dawley rats (n=24) were divided into two groups: group 1, control rats receiving vehicle (saline); group 2, rats receiving binge cocaine injections. After completion of triple-binge cocaine or saline injections, both groups underwent an in vivo, neurogenic-mediated erectile response protocol to assess intracavernosal pressure (ICP). Penile endothelin-A and -B receptors (ET(A)R and ET(B)R), plasma levels of big endothelin-1 (big-ET-1), and endothelial nitric oxide synthase (eNOS) protein expression were assessed. To analyze nitric oxide (NO) production, we measured plasma nitrate-nitrite levels and quantitated myeloperoxidase (MPO) activity in cavernosal tissues to determine reactive oxygen species generation. Endothelium-dependent and -independent relaxation responses were evaluated in vitro. Data were analyzed with Student t test. RESULTS: Triple-binge cocaine administration caused significantly decreased erectile responses as measured by ICP in vivo. Plasma big-ET-1 levels were significantly increased in the triple-binge cocaine treatment group compared with control animals. In the penis, triple-binge cocaine administration significantly increased ET(A)R expression compared with saline controls, while ET(B)R expression was not altered. Cocaine-treated rats had significantly decreased eNOS expression and NO production. The activity of tissue MPO was significantly increased in the cocaine group compared with control rats. Organ bath studies demonstrated that triple-binge cocaine resulted in a 64% reduction in maximal relaxation compared with the control group. CONCLUSION: This study demonstrates that triple-binge cocaine administration significantly reduces erectile function in rats. The pathophysiologic mechanisms that are likely involved include increased plasma big-ET-1 levels, increased penile ET(A)R expression, increased penile MPO activity, and reduced penile eNOS expression.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
EDN1Humanimpotence  ISOEdn1 (Rattus norvegicus)protein:increased expression:plasmaRGD 
EDNRAHumanimpotence  ISOEdnra (Rattus norvegicus) RGD 
Edn1Ratimpotence  IEP protein:increased expression:plasmaRGD 
Edn1Mouseimpotence  ISOEdn1 (Rattus norvegicus)protein:increased expression:plasmaRGD 
EdnraRatimpotence  IEP  RGD 
EdnraMouseimpotence  ISOEdnra (Rattus norvegicus) RGD 
NOS3Humanimpotence  ISONos3 (Rattus norvegicus)associated with Cocaine-Related Disorders and protein:decreased expression:penisRGD 
Nos3Ratimpotence  IEP associated with Cocaine-Related Disorders and protein:decreased expression:penisRGD 
Nos3Mouseimpotence  ISONos3 (Rattus norvegicus)associated with Cocaine-Related Disorders and protein:decreased expression:penisRGD 

Objects Annotated

Genes (Rattus norvegicus)
Edn1  (endothelin 1)
Ednra  (endothelin receptor type A)
Nos3  (nitric oxide synthase 3)

Genes (Mus musculus)
Edn1  (endothelin 1)
Ednra  (endothelin receptor type A)
Nos3  (nitric oxide synthase 3, endothelial cell)

Genes (Homo sapiens)
EDN1  (endothelin 1)
EDNRA  (endothelin receptor type A)
NOS3  (nitric oxide synthase 3)


Additional Information