Prostaglandin F2α but not latanoprost, increases the Ca2+ sensitivity of the pig iris sphincter muscle

Yuhei Hasegawa, Junji Nishimura, Naohisa Niiro, Katsuya Hirano, Tatsuro Ishibashi, Hideo Kanaide

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

PURPOSE. To determine the mechanisms underlying prostaglandin (PG) F 2α-, carbachol (CCh)-, or latanoprost (a PGF2α analogue)-induced contraction of the pig iris sphincter muscle. METHODS. Effects of these agents on myofilament Ca2+ sensitivity were evaluated and compared with the use of receptor-coupled permeabilized preparations by α-toxin. The effects of PGF2α and CCh on the phosphorylation of myosin light chain (MLC) were also analyzed. RESULTS. In the intact strips, all three of these agents induced contractions. In permeabilized strips, PGF2α and CCh, but not latanoprost, caused an additional tension development at a fixed intracellular Ca 2+ concentration ([Ca2+]i) and also shifted the [Ca2+]i-tension curve to the left, thus indicating that PGF2α and CCh, but not latanoprost, induced increases in Ca2+ sensitivity (Ca2+ sensitization). This Ca 2+ sensitization could have been inhibited by Y27632, a rho kinase inhibitor, but not by GF109203X, a protein kinase C (PKC) inhibitor or by PD98059, a mitogen-activated protein (MAP) kinase inhibitor. PGF 2α increased the level of MLC phosphorylation at a constant [Ca2+]i. CONCLUSIONS. PGF2α, but not latanoprost, induced Ca2+ sensitization of the pig iris sphincter muscle in an MLC phosphorylation-dependent manner through the rho-rho kinase pathway. The effect of latanoprost on the Ca2+ sensitization mechanism was different from that of PGF2α and was thought to play a beneficial role in glaucoma treatment.

Original languageEnglish
Pages (from-to)4865-4871
Number of pages7
JournalInvestigative Ophthalmology and Visual Science
Volume47
Issue number11
DOIs
Publication statusPublished - Nov 1 2006

Fingerprint

latanoprost
Dinoprost
Iris
Swine
Carbachol
Muscles
Myosin Light Chains
rho-Associated Kinases
Phosphorylation
Prostaglandins F
Protein Kinase Inhibitors
Protein C Inhibitor
Myofibrils
Mitogen-Activated Protein Kinases
Glaucoma
Protein Kinase C

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Prostaglandin F2α but not latanoprost, increases the Ca2+ sensitivity of the pig iris sphincter muscle. / Hasegawa, Yuhei; Nishimura, Junji; Niiro, Naohisa; Hirano, Katsuya; Ishibashi, Tatsuro; Kanaide, Hideo.

In: Investigative Ophthalmology and Visual Science, Vol. 47, No. 11, 01.11.2006, p. 4865-4871.

Research output: Contribution to journalArticle

Hasegawa, Yuhei ; Nishimura, Junji ; Niiro, Naohisa ; Hirano, Katsuya ; Ishibashi, Tatsuro ; Kanaide, Hideo. / Prostaglandin F2α but not latanoprost, increases the Ca2+ sensitivity of the pig iris sphincter muscle. In: Investigative Ophthalmology and Visual Science. 2006 ; Vol. 47, No. 11. pp. 4865-4871.
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abstract = "PURPOSE. To determine the mechanisms underlying prostaglandin (PG) F 2α-, carbachol (CCh)-, or latanoprost (a PGF2α analogue)-induced contraction of the pig iris sphincter muscle. METHODS. Effects of these agents on myofilament Ca2+ sensitivity were evaluated and compared with the use of receptor-coupled permeabilized preparations by α-toxin. The effects of PGF2α and CCh on the phosphorylation of myosin light chain (MLC) were also analyzed. RESULTS. In the intact strips, all three of these agents induced contractions. In permeabilized strips, PGF2α and CCh, but not latanoprost, caused an additional tension development at a fixed intracellular Ca 2+ concentration ([Ca2+]i) and also shifted the [Ca2+]i-tension curve to the left, thus indicating that PGF2α and CCh, but not latanoprost, induced increases in Ca2+ sensitivity (Ca2+ sensitization). This Ca 2+ sensitization could have been inhibited by Y27632, a rho kinase inhibitor, but not by GF109203X, a protein kinase C (PKC) inhibitor or by PD98059, a mitogen-activated protein (MAP) kinase inhibitor. PGF 2α increased the level of MLC phosphorylation at a constant [Ca2+]i. CONCLUSIONS. PGF2α, but not latanoprost, induced Ca2+ sensitization of the pig iris sphincter muscle in an MLC phosphorylation-dependent manner through the rho-rho kinase pathway. The effect of latanoprost on the Ca2+ sensitization mechanism was different from that of PGF2α and was thought to play a beneficial role in glaucoma treatment.",
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T1 - Prostaglandin F2α but not latanoprost, increases the Ca2+ sensitivity of the pig iris sphincter muscle

AU - Hasegawa, Yuhei

AU - Nishimura, Junji

AU - Niiro, Naohisa

AU - Hirano, Katsuya

AU - Ishibashi, Tatsuro

AU - Kanaide, Hideo

PY - 2006/11/1

Y1 - 2006/11/1

N2 - PURPOSE. To determine the mechanisms underlying prostaglandin (PG) F 2α-, carbachol (CCh)-, or latanoprost (a PGF2α analogue)-induced contraction of the pig iris sphincter muscle. METHODS. Effects of these agents on myofilament Ca2+ sensitivity were evaluated and compared with the use of receptor-coupled permeabilized preparations by α-toxin. The effects of PGF2α and CCh on the phosphorylation of myosin light chain (MLC) were also analyzed. RESULTS. In the intact strips, all three of these agents induced contractions. In permeabilized strips, PGF2α and CCh, but not latanoprost, caused an additional tension development at a fixed intracellular Ca 2+ concentration ([Ca2+]i) and also shifted the [Ca2+]i-tension curve to the left, thus indicating that PGF2α and CCh, but not latanoprost, induced increases in Ca2+ sensitivity (Ca2+ sensitization). This Ca 2+ sensitization could have been inhibited by Y27632, a rho kinase inhibitor, but not by GF109203X, a protein kinase C (PKC) inhibitor or by PD98059, a mitogen-activated protein (MAP) kinase inhibitor. PGF 2α increased the level of MLC phosphorylation at a constant [Ca2+]i. CONCLUSIONS. PGF2α, but not latanoprost, induced Ca2+ sensitization of the pig iris sphincter muscle in an MLC phosphorylation-dependent manner through the rho-rho kinase pathway. The effect of latanoprost on the Ca2+ sensitization mechanism was different from that of PGF2α and was thought to play a beneficial role in glaucoma treatment.

AB - PURPOSE. To determine the mechanisms underlying prostaglandin (PG) F 2α-, carbachol (CCh)-, or latanoprost (a PGF2α analogue)-induced contraction of the pig iris sphincter muscle. METHODS. Effects of these agents on myofilament Ca2+ sensitivity were evaluated and compared with the use of receptor-coupled permeabilized preparations by α-toxin. The effects of PGF2α and CCh on the phosphorylation of myosin light chain (MLC) were also analyzed. RESULTS. In the intact strips, all three of these agents induced contractions. In permeabilized strips, PGF2α and CCh, but not latanoprost, caused an additional tension development at a fixed intracellular Ca 2+ concentration ([Ca2+]i) and also shifted the [Ca2+]i-tension curve to the left, thus indicating that PGF2α and CCh, but not latanoprost, induced increases in Ca2+ sensitivity (Ca2+ sensitization). This Ca 2+ sensitization could have been inhibited by Y27632, a rho kinase inhibitor, but not by GF109203X, a protein kinase C (PKC) inhibitor or by PD98059, a mitogen-activated protein (MAP) kinase inhibitor. PGF 2α increased the level of MLC phosphorylation at a constant [Ca2+]i. CONCLUSIONS. PGF2α, but not latanoprost, induced Ca2+ sensitization of the pig iris sphincter muscle in an MLC phosphorylation-dependent manner through the rho-rho kinase pathway. The effect of latanoprost on the Ca2+ sensitization mechanism was different from that of PGF2α and was thought to play a beneficial role in glaucoma treatment.

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