Motilin induces the endothelium-dependent relaxation of smooth muscle and the elevation of cytosolic Calcium in endothelial cells in situ

Yoshihiro Higuchi, Junji Nishimura, Hideo Kanaide

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Abstract

Using front-surface fluorometry with fura-2 and porcine aortic valvular strips, we investigated the effect of motilin, a gastrointestinal peptide, on the cytosolic Ca2+ concentration ([Ca2+]i) of endothelial cells in situ. Motilin induced a biphasic elevation of [Ca2+]i of the endothelial cells on the porcine aortic valvular strips. To investigate the physiological role of these Ca2+ transients in the endothelial cells, we determined the effect of motilin on [Ca2+]i as well as the tension of the smooth muscles in the porcine coronary strips with an intact endothelium. Motilin decreased [Ca2+]i and the tension of the coronary smooth muscle precontracted by U46619, a thromboxane A2 analogue, in an endothelium-dependent manner. In the presence of indomethacin (a cycloxygenase inhibitor), motilin induced an endothelium-dependent relaxation of the coronary strips which was partially inhibited by Nω-nitro-L-arginine (L-NNA; a NO synthase inhibitor). These results thus indicate that motilin induces Ca2+ transients of the endothelial cells while it also induces vasorelaxation, which may be mediated by both L-NNA sensitive and resistant factors that are derived from the endothelium.

Original languageEnglish
Pages (from-to)346-353
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume202
Issue number1
DOIs
Publication statusPublished - Jul 15 1994

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Motilin
Endothelial cells
Endothelium
Smooth Muscle
Muscle
Endothelial Cells
Calcium
Swine
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Fluorometry
Thromboxane A2
Fura-2
Vasodilation
Nitric Oxide Synthase
Indomethacin
Arginine
Peptides

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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abstract = "Using front-surface fluorometry with fura-2 and porcine aortic valvular strips, we investigated the effect of motilin, a gastrointestinal peptide, on the cytosolic Ca2+ concentration ([Ca2+]i) of endothelial cells in situ. Motilin induced a biphasic elevation of [Ca2+]i of the endothelial cells on the porcine aortic valvular strips. To investigate the physiological role of these Ca2+ transients in the endothelial cells, we determined the effect of motilin on [Ca2+]i as well as the tension of the smooth muscles in the porcine coronary strips with an intact endothelium. Motilin decreased [Ca2+]i and the tension of the coronary smooth muscle precontracted by U46619, a thromboxane A2 analogue, in an endothelium-dependent manner. In the presence of indomethacin (a cycloxygenase inhibitor), motilin induced an endothelium-dependent relaxation of the coronary strips which was partially inhibited by Nω-nitro-L-arginine (L-NNA; a NO synthase inhibitor). These results thus indicate that motilin induces Ca2+ transients of the endothelial cells while it also induces vasorelaxation, which may be mediated by both L-NNA sensitive and resistant factors that are derived from the endothelium.",
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AU - Nishimura, Junji

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AB - Using front-surface fluorometry with fura-2 and porcine aortic valvular strips, we investigated the effect of motilin, a gastrointestinal peptide, on the cytosolic Ca2+ concentration ([Ca2+]i) of endothelial cells in situ. Motilin induced a biphasic elevation of [Ca2+]i of the endothelial cells on the porcine aortic valvular strips. To investigate the physiological role of these Ca2+ transients in the endothelial cells, we determined the effect of motilin on [Ca2+]i as well as the tension of the smooth muscles in the porcine coronary strips with an intact endothelium. Motilin decreased [Ca2+]i and the tension of the coronary smooth muscle precontracted by U46619, a thromboxane A2 analogue, in an endothelium-dependent manner. In the presence of indomethacin (a cycloxygenase inhibitor), motilin induced an endothelium-dependent relaxation of the coronary strips which was partially inhibited by Nω-nitro-L-arginine (L-NNA; a NO synthase inhibitor). These results thus indicate that motilin induces Ca2+ transients of the endothelial cells while it also induces vasorelaxation, which may be mediated by both L-NNA sensitive and resistant factors that are derived from the endothelium.

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