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Journal of vascular research1997; 34(2); 90-102; doi: 10.1159/000159206

Adrenoceptor-mediated regulation of the contractility in horse penile resistance arteries.

Abstract: The receptors mediating the contractions to both exogenously applied noradrenaline and electrical field stimulation (EFS) were characterized in horse isolated penile resistance arteries. The alpha 1-adrenoceptor-selective antagonist, prazosin, caused competitive rightward shifts of the contractile concentration-response curves (CRC) to phenylephrine. The alpha 2-antagonist, rauwolscine, also displaced to the right the CRC to the alpha 2-adrenoceptor-selective agonist, BHT 920. EFS (0.3 ms, 20-second trains) caused tetrodotoxin-sensitive frequency-dependent contractions which were enhanced in the presence of NG-nitro-L-arginine (L-NOARG, 3 x 10(-5) M), but not affected by mechanical endothelial cell removal. In experiments performed in the presence of L-NOARG, prazosin inhibited contractions to EFS, while rauwolscine inconsistently enhanced the contractile responses. Exogenously added noradrenaline induced contractions which were not changed in endothelium-denuded arteries, but significantly increased in the presence of L-NOARG. Prazosin inhibited the noradrenaline-induced contractions, while rauwolscine did not change the response to noradrenaline either alone or in the presence of prazosin. In the presence of phentolamine (10(-5) M), isoprenaline, adrenaline and the beta 2-adrenoceptor agonist, salbutamol, concentration-dependently relaxed penile resistance arteries, while the relaxations to noradrenaline and dobutamine, which activate beta 1-adrenoceptors, were negligible. Isoprenaline-induced relaxations were not changed in the presence of the beta 1-antagonist, atenolol (10(-7)-10(-6) M), but competitively inhibited by the beta 2-adrenoceptor antagonist, butoxamine (10(-6)-10(-5) M). The present results indicate that stimulation of adrenergic nerves in horse penile resistance arteries releases noradrenaline, which induces vasoconstriction through a predominant activation of alpha 1-adrenoceptors, while postjunctional alpha 2-adrenoceptors apparently play a minor role. Functional beta 2-adrenoceptors are also present in these arteries.
Publication Date: 1997-03-01 PubMed ID: 9167641DOI: 10.1159/000159206Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • P.H.S.

Summary

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The research investigates how adrenoceptors regulate the contractility in horse penile resistance arteries, demonstrating that alpha 1-adrenoceptors mainly instigate vasoconstriction while alpha 2-adrenoceptors play a minimal role and beta 2-adrenoceptors are also present with their function.

Understanding the Terms

  • Adrenoceptor: These are a type of protein found in various tissues of the body like smooth muscles, heart, and lungs, which respond to adrenaline or noradrenaline inducing a physiological response.
  • Noradrenaline: It is a hormone and neurotransmitter involved in the body’s response to stress and anxiety, triggering constriction of blood vessels and increasing blood pressure.
  • Electrical Field Stimulation (EFS): A research method using electric current to stimulate nerves.
  • Alpha 1-adrenoceptor, Alpha 2-adrenoceptor, Beta 1-adrenoceptor, Beta 2-adrenoceptor: These are subtypes of adrenoceptors, responding to adrenaline or noradrenaline differently and inducing different physiological reactions.

Research Methods and Findings

  • The study used horse isolated penile resistance arteries to characterize the receptors mediating contractions in response to noradrenaline and Electrical Field Stimulation (EFS).
  • Various antagonist drugs (prazosin, rauwolscine) were used to inhibit different adrenoceptors and observe their impact on contractile responses.
  • EFS induced contractions were found to be frequency-dependent, heightened by the presence of L-NOARG (a nitric oxide synthase inhibitor) but unaffected by mechanical removal of endothelial cells. Prazosin consistently inhibited these contractile responses to EFS.
  • Similar experiments with exogenous noradrenaline found that prazosin also inhibited these induced contractions, and endothelium removal didn’t affect these contractions.
  • When phentolamine was present, isoprenaline, adrenaline, and the beta 2-adrenoceptor agonist, salbutamol, induced relaxation in penile resistance arteries, indicating the presence and function of beta 2-adrenoceptors in these arteries.

Core Conclusions

  • The research suggests that noradrenaline, released through the stimulation of adrenergic nerves in horse penile resistance arteries, causes vasoconstriction primarily via the activation of alpha 1-adrenoceptors.
  • Postjunctional alpha 2-adrenoceptors appear to play a more minor role in this setting, evidenced by the inconsistent enhancement of contraction responses when rauwolscine displaces CRCs.
  • Functional beta 2-adrenoceptors also exist in these arteries, supported by the relaxation response witnessed when beta 2-adrenoceptor agonists are administered.

Cite This Article

APA
Simonsen U, Prieto D, Hernández M, Sáenz de Tejada I, García-Sacristán A. (1997). Adrenoceptor-mediated regulation of the contractility in horse penile resistance arteries. J Vasc Res, 34(2), 90-102. https://doi.org/10.1159/000159206

Publication

ISSN: 1018-1172
NlmUniqueID: 9206092
Country: Switzerland
Language: English
Volume: 34
Issue: 2
Pages: 90-102

Researcher Affiliations

Simonsen, U
  • Departamento de Fisiología, Facultad de Veterinaria, Universidad Complutense, Madrid, Spain. US@farm.aau.dk
Prieto, D
    Hernández, M
      Sáenz de Tejada, I
        García-Sacristán, A

          MeSH Terms

          • Animals
          • Electric Stimulation
          • Endothelium, Vascular / physiology
          • Horses
          • Male
          • Nitric Oxide / physiology
          • Norepinephrine / physiology
          • Penis / blood supply
          • Receptors, Adrenergic, alpha / physiology
          • Receptors, Adrenergic, beta / physiology
          • Signal Transduction
          • Vascular Resistance
          • Vasoconstriction

          Grant Funding

          • R01-DK-39080 / NIDDK NIH HHS
          • R01-DK-40487 / NIDDK NIH HHS

          Citations

          This article has been cited 3 times.
          1. Contreras C, Sánchez A, Martínez P, Raposo R, Climent B, García-Sacristán A, Benedito S, Prieto D. Insulin resistance in penile arteries from a rat model of metabolic syndrome. Br J Pharmacol 2010 Sep;161(2):350-64.
          2. Prieto D, Arcos LR, Martínez P, Benedito S, García-Sacristán A, Hernández M. Heterogeneity of the neuropeptide Y (NPY) contractile and relaxing receptors in horse penile small arteries. Br J Pharmacol 2004 Dec;143(8):976-86.
            doi: 10.1038/sj.bjp.0706005pubmed: 15557288google scholar: lookup
          3. Mizusawa H, Hedlund P, Sjunnesson J, Brioni JD, Sullivan JP, Andersson KE. Enhancement of apomorphine-induced penile erection in the rat by a selective alpha(1D)-adrenoceptor antagonist. Br J Pharmacol 2002 Jul;136(5):701-8.
            doi: 10.1038/sj.bjp.0704773pubmed: 12086979google scholar: lookup