The action mechanism of relaxation effect of atropine on the isolated rabbit corpus cavernosum

Youngdeuk Choi, Woo Sik Chung, Hyung Ki Choi

Research output: Contribution to journalArticle

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Abstract

Purpose: Atropine has been used to block cholinergic neurotransmission in basic research and has received recent interest clinically in the intracavernosal pharmacotherapy of erectile dysfunction. It has been suggested that at a low dose (10-8 M), atropine blocks muscarinic receptors, and that at a large dose (10-3 M), it induces the release of EDRF. However, no report has supported this idea experimentally. We tried to confirm the action of atropine in cavernosal tissue and define its mechanism. Materials and Methods: Strips of rabbit corpus cavernosum were mounted in organ chambers. On the precontracted muscle strips with phenylephrine (PHE; 5 x 10-6 M), atropine was treated with increasing concentration from 10-11 M. The relaxing activity of atropine was observed in deendothelialized tissue and preparation with treatment with methylene blue (10-4 M), pyrogallol (10-4 M), N(W)-nitro-L-arginine (L-NNA; 3 x 10-4 M) and indomethacin (10-4 M). To evaluate the relationship of atropine to Ca++, the muscle strip was incubated in Ca++ free solution, and Ca++ induced contraction by addition of CaCl2 (10-3 M) was recorded with atropine. Depolarization by KCl was observed with atropine to investigate the relationship of atropine relaxation to K+. Results: On the precontracted muscle strip with PHE, atropine induced a dose-related contraction up to 10-8 M and began to exert a relaxing effect at the concentration of 10-7 M and reached the 93.6% relaxation effect at the concentration of 10-4 M, causing dose-dependent relaxation. The relaxing effect of atropine was partially inhibited by endothelial disruption, and by pretreatment with methylene blue, pyrogallol, L-NNA, and indomethacin, although they were not statistically significant. At the basal state of muscle strips in Ca++ free solution, atropine decreased basal tension as well as inhibited the contraction induced by CaCl2 dose- dependently. However, atropine did not influence depolarization by KCl. Conclusions: Atropine has both a contraction effect at lower concentrations and a relaxation effect at higher concentrations on cavernosal smooth muscle. It is presumed that the relaxation at higher concentrations is mediated via increasing intracellular calcium sequestration, not by hyperpolarization or secretion of EDRF.

Original languageEnglish
Pages (from-to)1976-1979
Number of pages4
JournalJournal of Urology
Volume161
Issue number6
DOIs
Publication statusPublished - 1999 Jan 1

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Atropine
Rabbits
Pyrogallol
Muscles
Methylene Blue
Indomethacin
Phenylephrine
Muscarinic Receptors
Erectile Dysfunction
Synaptic Transmission
Cholinergic Agents
Smooth Muscle
Arginine

All Science Journal Classification (ASJC) codes

  • Urology

Cite this

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title = "The action mechanism of relaxation effect of atropine on the isolated rabbit corpus cavernosum",
abstract = "Purpose: Atropine has been used to block cholinergic neurotransmission in basic research and has received recent interest clinically in the intracavernosal pharmacotherapy of erectile dysfunction. It has been suggested that at a low dose (10-8 M), atropine blocks muscarinic receptors, and that at a large dose (10-3 M), it induces the release of EDRF. However, no report has supported this idea experimentally. We tried to confirm the action of atropine in cavernosal tissue and define its mechanism. Materials and Methods: Strips of rabbit corpus cavernosum were mounted in organ chambers. On the precontracted muscle strips with phenylephrine (PHE; 5 x 10-6 M), atropine was treated with increasing concentration from 10-11 M. The relaxing activity of atropine was observed in deendothelialized tissue and preparation with treatment with methylene blue (10-4 M), pyrogallol (10-4 M), N(W)-nitro-L-arginine (L-NNA; 3 x 10-4 M) and indomethacin (10-4 M). To evaluate the relationship of atropine to Ca++, the muscle strip was incubated in Ca++ free solution, and Ca++ induced contraction by addition of CaCl2 (10-3 M) was recorded with atropine. Depolarization by KCl was observed with atropine to investigate the relationship of atropine relaxation to K+. Results: On the precontracted muscle strip with PHE, atropine induced a dose-related contraction up to 10-8 M and began to exert a relaxing effect at the concentration of 10-7 M and reached the 93.6{\%} relaxation effect at the concentration of 10-4 M, causing dose-dependent relaxation. The relaxing effect of atropine was partially inhibited by endothelial disruption, and by pretreatment with methylene blue, pyrogallol, L-NNA, and indomethacin, although they were not statistically significant. At the basal state of muscle strips in Ca++ free solution, atropine decreased basal tension as well as inhibited the contraction induced by CaCl2 dose- dependently. However, atropine did not influence depolarization by KCl. Conclusions: Atropine has both a contraction effect at lower concentrations and a relaxation effect at higher concentrations on cavernosal smooth muscle. It is presumed that the relaxation at higher concentrations is mediated via increasing intracellular calcium sequestration, not by hyperpolarization or secretion of EDRF.",
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The action mechanism of relaxation effect of atropine on the isolated rabbit corpus cavernosum. / Choi, Youngdeuk; Chung, Woo Sik; Choi, Hyung Ki.

In: Journal of Urology, Vol. 161, No. 6, 01.01.1999, p. 1976-1979.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The action mechanism of relaxation effect of atropine on the isolated rabbit corpus cavernosum

AU - Choi, Youngdeuk

AU - Chung, Woo Sik

AU - Choi, Hyung Ki

PY - 1999/1/1

Y1 - 1999/1/1

N2 - Purpose: Atropine has been used to block cholinergic neurotransmission in basic research and has received recent interest clinically in the intracavernosal pharmacotherapy of erectile dysfunction. It has been suggested that at a low dose (10-8 M), atropine blocks muscarinic receptors, and that at a large dose (10-3 M), it induces the release of EDRF. However, no report has supported this idea experimentally. We tried to confirm the action of atropine in cavernosal tissue and define its mechanism. Materials and Methods: Strips of rabbit corpus cavernosum were mounted in organ chambers. On the precontracted muscle strips with phenylephrine (PHE; 5 x 10-6 M), atropine was treated with increasing concentration from 10-11 M. The relaxing activity of atropine was observed in deendothelialized tissue and preparation with treatment with methylene blue (10-4 M), pyrogallol (10-4 M), N(W)-nitro-L-arginine (L-NNA; 3 x 10-4 M) and indomethacin (10-4 M). To evaluate the relationship of atropine to Ca++, the muscle strip was incubated in Ca++ free solution, and Ca++ induced contraction by addition of CaCl2 (10-3 M) was recorded with atropine. Depolarization by KCl was observed with atropine to investigate the relationship of atropine relaxation to K+. Results: On the precontracted muscle strip with PHE, atropine induced a dose-related contraction up to 10-8 M and began to exert a relaxing effect at the concentration of 10-7 M and reached the 93.6% relaxation effect at the concentration of 10-4 M, causing dose-dependent relaxation. The relaxing effect of atropine was partially inhibited by endothelial disruption, and by pretreatment with methylene blue, pyrogallol, L-NNA, and indomethacin, although they were not statistically significant. At the basal state of muscle strips in Ca++ free solution, atropine decreased basal tension as well as inhibited the contraction induced by CaCl2 dose- dependently. However, atropine did not influence depolarization by KCl. Conclusions: Atropine has both a contraction effect at lower concentrations and a relaxation effect at higher concentrations on cavernosal smooth muscle. It is presumed that the relaxation at higher concentrations is mediated via increasing intracellular calcium sequestration, not by hyperpolarization or secretion of EDRF.

AB - Purpose: Atropine has been used to block cholinergic neurotransmission in basic research and has received recent interest clinically in the intracavernosal pharmacotherapy of erectile dysfunction. It has been suggested that at a low dose (10-8 M), atropine blocks muscarinic receptors, and that at a large dose (10-3 M), it induces the release of EDRF. However, no report has supported this idea experimentally. We tried to confirm the action of atropine in cavernosal tissue and define its mechanism. Materials and Methods: Strips of rabbit corpus cavernosum were mounted in organ chambers. On the precontracted muscle strips with phenylephrine (PHE; 5 x 10-6 M), atropine was treated with increasing concentration from 10-11 M. The relaxing activity of atropine was observed in deendothelialized tissue and preparation with treatment with methylene blue (10-4 M), pyrogallol (10-4 M), N(W)-nitro-L-arginine (L-NNA; 3 x 10-4 M) and indomethacin (10-4 M). To evaluate the relationship of atropine to Ca++, the muscle strip was incubated in Ca++ free solution, and Ca++ induced contraction by addition of CaCl2 (10-3 M) was recorded with atropine. Depolarization by KCl was observed with atropine to investigate the relationship of atropine relaxation to K+. Results: On the precontracted muscle strip with PHE, atropine induced a dose-related contraction up to 10-8 M and began to exert a relaxing effect at the concentration of 10-7 M and reached the 93.6% relaxation effect at the concentration of 10-4 M, causing dose-dependent relaxation. The relaxing effect of atropine was partially inhibited by endothelial disruption, and by pretreatment with methylene blue, pyrogallol, L-NNA, and indomethacin, although they were not statistically significant. At the basal state of muscle strips in Ca++ free solution, atropine decreased basal tension as well as inhibited the contraction induced by CaCl2 dose- dependently. However, atropine did not influence depolarization by KCl. Conclusions: Atropine has both a contraction effect at lower concentrations and a relaxation effect at higher concentrations on cavernosal smooth muscle. It is presumed that the relaxation at higher concentrations is mediated via increasing intracellular calcium sequestration, not by hyperpolarization or secretion of EDRF.

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