抄録
We have investigated the effect of phorbol esters and the down-regulation of protein kinase C on contraction of guinea-pig ileum longitudinal smooth muscle to carbachol and high K+. Phorbol 12,13-dibutyrate (PDBu) enhanced the phasic component and inhibited or enhanced, respectively, the tonic component of contraction to carbachol and high K+. In contrast, 4α-phorbol, which does not activate protein kinase C, had no effect on these responses. Exposure to phorbol 12-myristate 13-acetate (PMA; 1 μM) for up to 8 h induced a time-dependent loss of [3H]-PDBu binding sites, consistent with the down-regulation of protein kinase C by this treatment. The phasic component of contraction to carbachol or high K+ was unaffected following the down-regulation of protein kinase C. The tonic component of contraction to carbachol was markedly enhanced by this treatment while that to high K+ was partially suppressed. These data suggest that although the activation of protein kinase C can lead to potentiation of the phasic component of contraction to carbachol or high K+, this appears to have little physiological significance since the response is not altered in tissues in which protein kinase C has been down-regulated. On the other hand, protein kinase C may limit the tonic contraction to carbachol but potentiate that to high K+.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 791-798 |
| ページ数 | 8 |
| ジャーナル | British Journal of Pharmacology |
| 巻 | 98 |
| 発行部数 | 3 |
| DOI | |
| 出版物ステータス | 出版済み - 1 1 1989 |
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All Science Journal Classification (ASJC) codes
- Pharmacology
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Protein kinase C regulates the tonic but not the phasic component of contraction in guinea-pig ileum. / Sasaguri, T.; Watson, S. P.
：: British Journal of Pharmacology, 巻 98, 番号 3, 01.01.1989, p. 791-798.研究成果: ジャーナルへの寄稿 › 記事
}
TY - JOUR
T1 - Protein kinase C regulates the tonic but not the phasic component of contraction in guinea-pig ileum
AU - Sasaguri, T.
AU - Watson, S. P.
PY - 1989/1/1
Y1 - 1989/1/1
N2 - We have investigated the effect of phorbol esters and the down-regulation of protein kinase C on contraction of guinea-pig ileum longitudinal smooth muscle to carbachol and high K+. Phorbol 12,13-dibutyrate (PDBu) enhanced the phasic component and inhibited or enhanced, respectively, the tonic component of contraction to carbachol and high K+. In contrast, 4α-phorbol, which does not activate protein kinase C, had no effect on these responses. Exposure to phorbol 12-myristate 13-acetate (PMA; 1 μM) for up to 8 h induced a time-dependent loss of [3H]-PDBu binding sites, consistent with the down-regulation of protein kinase C by this treatment. The phasic component of contraction to carbachol or high K+ was unaffected following the down-regulation of protein kinase C. The tonic component of contraction to carbachol was markedly enhanced by this treatment while that to high K+ was partially suppressed. These data suggest that although the activation of protein kinase C can lead to potentiation of the phasic component of contraction to carbachol or high K+, this appears to have little physiological significance since the response is not altered in tissues in which protein kinase C has been down-regulated. On the other hand, protein kinase C may limit the tonic contraction to carbachol but potentiate that to high K+.
AB - We have investigated the effect of phorbol esters and the down-regulation of protein kinase C on contraction of guinea-pig ileum longitudinal smooth muscle to carbachol and high K+. Phorbol 12,13-dibutyrate (PDBu) enhanced the phasic component and inhibited or enhanced, respectively, the tonic component of contraction to carbachol and high K+. In contrast, 4α-phorbol, which does not activate protein kinase C, had no effect on these responses. Exposure to phorbol 12-myristate 13-acetate (PMA; 1 μM) for up to 8 h induced a time-dependent loss of [3H]-PDBu binding sites, consistent with the down-regulation of protein kinase C by this treatment. The phasic component of contraction to carbachol or high K+ was unaffected following the down-regulation of protein kinase C. The tonic component of contraction to carbachol was markedly enhanced by this treatment while that to high K+ was partially suppressed. These data suggest that although the activation of protein kinase C can lead to potentiation of the phasic component of contraction to carbachol or high K+, this appears to have little physiological significance since the response is not altered in tissues in which protein kinase C has been down-regulated. On the other hand, protein kinase C may limit the tonic contraction to carbachol but potentiate that to high K+.
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UR - http://www.scopus.com/inward/citedby.url?scp=0024460735&partnerID=8YFLogxK
U2 - 10.1111/j.1476-5381.1989.tb14607.x
DO - 10.1111/j.1476-5381.1989.tb14607.x
M3 - Article
C2 - 2590770
AN - SCOPUS:0024460735
VL - 98
SP - 791
EP - 798
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 3
ER -