Involvement of nitric oxide and vasoactive intestinal peptide in the nonadrenergic-noncholinergic relaxation of the porcine retractor penis muscle

Jun-Ho La, T. Kim, T. Sung, T. Kang, J. Lee, I. Yang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Neurotransmitters mediating nonadrenergic-noncholinergic (NANC) relaxation were investigated in strips of porcine retractor penis muscle (RPM). Muscle tone was raised by phenylephrine (1 μM) in the presence of atropine (1 μM) and guanethidine (50 μM). Upon electrical field stimulation (1 ms, 80 V, 1 - 32 Hz for 10 s), the initial fast relaxation was followed by the slow relaxation. Although the fast and the slow relaxation were completely abolished by tetrodotoxin (1 μM), they showed different pharmacological sensitivities to the nitric oxide (NO) synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME, 0.1 mM). The fast relaxation was markedly inhibited by L-NAME in an L-arginine reversible manner and by oxyhemoglobin (50 μM), while the slow relaxation was hardly blocked by L-NAME. L-NAME and α-chymotrypsin (α-CT, 3 U/ml) selectively inhibited the fast and the slow relaxation, respectively. α-CT abolished L-NAME-resistant slow relaxation, and L-NAME completely abolished the α-CT-resistant fast relaxation. α-CT-resistant relaxation was not significantly different from the digitally calculated L-NAME-sensitive component, and L-NAME-resistant relaxation was similar to the digitally calculated α-CT-sensitive component. Vasoactive intestinal peptide (VIP, 0.003 - 0.1 μM) relaxed porcine RPM in a concentration-dependent manner. The effect of a VIP was partially inhibited by a VIP receptor antagonist, VIP(10 - 28) (1 and 3 μM). L-NAME-resistant relaxation was also reduced by VIP(10 - 28) (3 μM) and by another putative antagonist, VIP(6 - 28) (1 μM), although the effects of the two antagonists were somewhat inconsistent. From the histochemical staining, it was verified that nerve bundles that showed VIP-like immunoreactivities were also positive for the NADPH diaphorase reaction. These results suggest that NO and peptide neurotransmitter(s) including VIP mediate the NANC relaxation in porcine RPM.

Original languageEnglish (US)
Pages (from-to)236-243
Number of pages8
JournalJapanese Journal of Pharmacology
Volume86
Issue number2
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Vasoactive Intestinal Peptide
NG-Nitroarginine Methyl Ester
Penis
Nitric Oxide
Swine
Muscles
Neurotransmitter Agents
Vasoactive Intestinal Peptide Receptors
NADPH Dehydrogenase
Guanethidine
Oxyhemoglobins
Tetrodotoxin
Chymotrypsin
Phenylephrine
Atropine
Nitric Oxide Synthase
Electric Stimulation
Arginine
Pharmacology
Staining and Labeling

Keywords

  • Boar
  • Nitric oxide
  • Retractor penis muscle
  • Vasoactive intestinal peptide

ASJC Scopus subject areas

  • Pharmacology
  • Molecular Medicine

Cite this

Involvement of nitric oxide and vasoactive intestinal peptide in the nonadrenergic-noncholinergic relaxation of the porcine retractor penis muscle. / La, Jun-Ho; Kim, T.; Sung, T.; Kang, T.; Lee, J.; Yang, I.

In: Japanese Journal of Pharmacology, Vol. 86, No. 2, 2001, p. 236-243.

Research output: Contribution to journalArticle

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AU - Kang, T.

AU - Lee, J.

AU - Yang, I.

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AB - Neurotransmitters mediating nonadrenergic-noncholinergic (NANC) relaxation were investigated in strips of porcine retractor penis muscle (RPM). Muscle tone was raised by phenylephrine (1 μM) in the presence of atropine (1 μM) and guanethidine (50 μM). Upon electrical field stimulation (1 ms, 80 V, 1 - 32 Hz for 10 s), the initial fast relaxation was followed by the slow relaxation. Although the fast and the slow relaxation were completely abolished by tetrodotoxin (1 μM), they showed different pharmacological sensitivities to the nitric oxide (NO) synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME, 0.1 mM). The fast relaxation was markedly inhibited by L-NAME in an L-arginine reversible manner and by oxyhemoglobin (50 μM), while the slow relaxation was hardly blocked by L-NAME. L-NAME and α-chymotrypsin (α-CT, 3 U/ml) selectively inhibited the fast and the slow relaxation, respectively. α-CT abolished L-NAME-resistant slow relaxation, and L-NAME completely abolished the α-CT-resistant fast relaxation. α-CT-resistant relaxation was not significantly different from the digitally calculated L-NAME-sensitive component, and L-NAME-resistant relaxation was similar to the digitally calculated α-CT-sensitive component. Vasoactive intestinal peptide (VIP, 0.003 - 0.1 μM) relaxed porcine RPM in a concentration-dependent manner. The effect of a VIP was partially inhibited by a VIP receptor antagonist, VIP(10 - 28) (1 and 3 μM). L-NAME-resistant relaxation was also reduced by VIP(10 - 28) (3 μM) and by another putative antagonist, VIP(6 - 28) (1 μM), although the effects of the two antagonists were somewhat inconsistent. From the histochemical staining, it was verified that nerve bundles that showed VIP-like immunoreactivities were also positive for the NADPH diaphorase reaction. These results suggest that NO and peptide neurotransmitter(s) including VIP mediate the NANC relaxation in porcine RPM.

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