Murine and rat cavernosal responses to endothelin-1 and urotensin-II Vasoactive Peptide Symposium

Fernando S. Carneiro, Zidonia N. Carneiro, Fernanda R.C. Giachini, Victor V. Lima, Edson F. Nogueira, William E. Rainey, Rita C. Tostes, R. Clinton Webb

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Endothelin-1 (ET-1) and urotensin-II (U-II) are the most potent constrictors of human vessels. Although the cavernosal tissue is highly responsive to ET-1, no information exists on the effects of U-II on cavernosal function. The aim of this study was to characterize ET-1 and U-II responses in corpora cavernosa from rats and mice. Male Wistar rats and C57/BL6 mice were used at 13 weeks. Cumulative concentration-response curves to ET-1, U-II, and IRL-1620, an ETB agonist, were performed. ET-1 increased force generation in cavernosal strips from mice and rats, but no response to U-II was observed in the presence or absence of Nω-nitro-L-arginine methyl ester (L-NAME), or in strips prestimulated with 20 mM KCl. IRL-1620 did not induce cavernosal contraction even in presence of L-NAME, but induced a cavernosal relaxation that was greater in rats than mice. No relaxation responses to U-II were observed in cavernosal strips precontracted with phenylephrine. mRNA expression of ET-1, ETA, ETB, and U-II receptors, but not U-II was observed in cavernosal strips. ET-1, via ETA receptors activation, causes contractile responses in cavernosal strips from rats and mice, whereas ETB receptor activation produces relaxation. Although the cavernosal tissue expresses U-II receptors, U-II does not induce contractile responses in corpora cavernosa from mice or rats.

Original languageEnglish (US)
Pages (from-to)439-447
Number of pages9
JournalJournal of the American Society of Hypertension
Issue number6
StatePublished - Nov 2008


  • DOCA-salt hypertension
  • ET receptor
  • corpus cavernosum
  • erectile dysfunction

ASJC Scopus subject areas

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine


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