Ca2+ influx in the endothelial cells is required for the bradykinin-induced endothelium-dependent contraction in the porcine interlobar renal artery

Eikichi Ihara, Dmitry N. Derkach, Katsuya Hirano, Junji Nishimura, Hajime Nawata, Hideo Kanaide

研究成果: ジャーナルへの寄稿記事

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1. To determine the mechanism of bradykinin-induced production of endothelium-derived contracting factors, we monitored the changes in cytosolic Ca2+ concentration ([Ca2+]i) in in situ endothelial cells in porcine aortic valvular strips and the changes in [Ca2+]i of smooth muscle cells and force in porcine interlobar renal arterial strips using front-surface fluorometry of fura-2. 2. In the presence of Nω-nitro-L-arginine methyl ester, bradykinin caused an endothelium-dependent transient elevation of [Ca2+]i and contraction in smooth muscle in the interlobar renal artery. This contraction was completely inhibited by a prostaglandin H2/thromboxane A2 receptor antagonist. 3. In the absence of extracellular Ca2+, bradykinin failed to induce contraction. However, replenishing extracellular Ca2+ to 0.75 mM and higher induced an instantaneous contraction. However, replenishing Ca2+ per se did not induce any contraction in the absence of bradykinin. Pretreatment with either 10-5 M 1-(β-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF96365) or 0.2 mM Ni2+ abolished the contraction induced by bradykinin in the presence of extracellular Ca2+. 4. Treatment with 10-5 M indomethacin completely inhibited the contractile response induced by Ca2+ replenishment, regardless of the timing of its application, before or after the application of bradykinin. 5. In endothelial cells in the valvular strips, bradykinin caused a transient [Ca2+]i elevation in the presence of 1.25 mM extracellular Ca2+, but [Ca2+]i returned to the resting level within 10 min. Neither 10-5 M SKF96365 nor 0.2mM Ni2+ had any effect on the peak [Ca2+]i elevation, but decreased [Ca2+]i in the declining phase. In the absence of extracellular Ca2+, bradykinin induced a transient [Ca2+]i elevation to a level similar to that seen in the presence of 1.25 mM extracellular Ca2+. However, [Ca2+]i then rapidly returned to the prestimulation level within 5 min. Subsequent Ca2+ replenishment to 0.75 mM and higher in the presence of bradykinin elevated [Ca2+]i to significantly higher levels than the resting level seen in the media containing 1.25 mM Ca2+. 6. In conclusion, Ca2+ influx in the endothelial cells is essential for bradykinin to induce endothelium-dependent contraction in the porcine interlobar renal artery.

元の言語英語
ページ(範囲)701-711
ページ数11
ジャーナルJournal of Physiology
534
発行部数3
DOI
出版物ステータス出版済み - 8 1 2001

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Bradykinin
Renal Artery
Endothelium
Swine
Endothelial Cells
1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
Prostaglandin H2 Receptors Thromboxane A2
Fluorometry
Fura-2
Indomethacin
Smooth Muscle Myocytes
Smooth Muscle
Kidney

All Science Journal Classification (ASJC) codes

  • Physiology

これを引用

Ca2+ influx in the endothelial cells is required for the bradykinin-induced endothelium-dependent contraction in the porcine interlobar renal artery. / Ihara, Eikichi; Derkach, Dmitry N.; Hirano, Katsuya; Nishimura, Junji; Nawata, Hajime; Kanaide, Hideo.

:: Journal of Physiology, 巻 534, 番号 3, 01.08.2001, p. 701-711.

研究成果: ジャーナルへの寄稿記事

Ihara, Eikichi ; Derkach, Dmitry N. ; Hirano, Katsuya ; Nishimura, Junji ; Nawata, Hajime ; Kanaide, Hideo. / Ca2+ influx in the endothelial cells is required for the bradykinin-induced endothelium-dependent contraction in the porcine interlobar renal artery. :: Journal of Physiology. 2001 ; 巻 534, 番号 3. pp. 701-711.
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abstract = "1. To determine the mechanism of bradykinin-induced production of endothelium-derived contracting factors, we monitored the changes in cytosolic Ca2+ concentration ([Ca2+]i) in in situ endothelial cells in porcine aortic valvular strips and the changes in [Ca2+]i of smooth muscle cells and force in porcine interlobar renal arterial strips using front-surface fluorometry of fura-2. 2. In the presence of Nω-nitro-L-arginine methyl ester, bradykinin caused an endothelium-dependent transient elevation of [Ca2+]i and contraction in smooth muscle in the interlobar renal artery. This contraction was completely inhibited by a prostaglandin H2/thromboxane A2 receptor antagonist. 3. In the absence of extracellular Ca2+, bradykinin failed to induce contraction. However, replenishing extracellular Ca2+ to 0.75 mM and higher induced an instantaneous contraction. However, replenishing Ca2+ per se did not induce any contraction in the absence of bradykinin. Pretreatment with either 10-5 M 1-(β-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF96365) or 0.2 mM Ni2+ abolished the contraction induced by bradykinin in the presence of extracellular Ca2+. 4. Treatment with 10-5 M indomethacin completely inhibited the contractile response induced by Ca2+ replenishment, regardless of the timing of its application, before or after the application of bradykinin. 5. In endothelial cells in the valvular strips, bradykinin caused a transient [Ca2+]i elevation in the presence of 1.25 mM extracellular Ca2+, but [Ca2+]i returned to the resting level within 10 min. Neither 10-5 M SKF96365 nor 0.2mM Ni2+ had any effect on the peak [Ca2+]i elevation, but decreased [Ca2+]i in the declining phase. In the absence of extracellular Ca2+, bradykinin induced a transient [Ca2+]i elevation to a level similar to that seen in the presence of 1.25 mM extracellular Ca2+. However, [Ca2+]i then rapidly returned to the prestimulation level within 5 min. Subsequent Ca2+ replenishment to 0.75 mM and higher in the presence of bradykinin elevated [Ca2+]i to significantly higher levels than the resting level seen in the media containing 1.25 mM Ca2+. 6. In conclusion, Ca2+ influx in the endothelial cells is essential for bradykinin to induce endothelium-dependent contraction in the porcine interlobar renal artery.",
author = "Eikichi Ihara and Derkach, {Dmitry N.} and Katsuya Hirano and Junji Nishimura and Hajime Nawata and Hideo Kanaide",
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T1 - Ca2+ influx in the endothelial cells is required for the bradykinin-induced endothelium-dependent contraction in the porcine interlobar renal artery

AU - Ihara, Eikichi

AU - Derkach, Dmitry N.

AU - Hirano, Katsuya

AU - Nishimura, Junji

AU - Nawata, Hajime

AU - Kanaide, Hideo

PY - 2001/8/1

Y1 - 2001/8/1

N2 - 1. To determine the mechanism of bradykinin-induced production of endothelium-derived contracting factors, we monitored the changes in cytosolic Ca2+ concentration ([Ca2+]i) in in situ endothelial cells in porcine aortic valvular strips and the changes in [Ca2+]i of smooth muscle cells and force in porcine interlobar renal arterial strips using front-surface fluorometry of fura-2. 2. In the presence of Nω-nitro-L-arginine methyl ester, bradykinin caused an endothelium-dependent transient elevation of [Ca2+]i and contraction in smooth muscle in the interlobar renal artery. This contraction was completely inhibited by a prostaglandin H2/thromboxane A2 receptor antagonist. 3. In the absence of extracellular Ca2+, bradykinin failed to induce contraction. However, replenishing extracellular Ca2+ to 0.75 mM and higher induced an instantaneous contraction. However, replenishing Ca2+ per se did not induce any contraction in the absence of bradykinin. Pretreatment with either 10-5 M 1-(β-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF96365) or 0.2 mM Ni2+ abolished the contraction induced by bradykinin in the presence of extracellular Ca2+. 4. Treatment with 10-5 M indomethacin completely inhibited the contractile response induced by Ca2+ replenishment, regardless of the timing of its application, before or after the application of bradykinin. 5. In endothelial cells in the valvular strips, bradykinin caused a transient [Ca2+]i elevation in the presence of 1.25 mM extracellular Ca2+, but [Ca2+]i returned to the resting level within 10 min. Neither 10-5 M SKF96365 nor 0.2mM Ni2+ had any effect on the peak [Ca2+]i elevation, but decreased [Ca2+]i in the declining phase. In the absence of extracellular Ca2+, bradykinin induced a transient [Ca2+]i elevation to a level similar to that seen in the presence of 1.25 mM extracellular Ca2+. However, [Ca2+]i then rapidly returned to the prestimulation level within 5 min. Subsequent Ca2+ replenishment to 0.75 mM and higher in the presence of bradykinin elevated [Ca2+]i to significantly higher levels than the resting level seen in the media containing 1.25 mM Ca2+. 6. In conclusion, Ca2+ influx in the endothelial cells is essential for bradykinin to induce endothelium-dependent contraction in the porcine interlobar renal artery.

AB - 1. To determine the mechanism of bradykinin-induced production of endothelium-derived contracting factors, we monitored the changes in cytosolic Ca2+ concentration ([Ca2+]i) in in situ endothelial cells in porcine aortic valvular strips and the changes in [Ca2+]i of smooth muscle cells and force in porcine interlobar renal arterial strips using front-surface fluorometry of fura-2. 2. In the presence of Nω-nitro-L-arginine methyl ester, bradykinin caused an endothelium-dependent transient elevation of [Ca2+]i and contraction in smooth muscle in the interlobar renal artery. This contraction was completely inhibited by a prostaglandin H2/thromboxane A2 receptor antagonist. 3. In the absence of extracellular Ca2+, bradykinin failed to induce contraction. However, replenishing extracellular Ca2+ to 0.75 mM and higher induced an instantaneous contraction. However, replenishing Ca2+ per se did not induce any contraction in the absence of bradykinin. Pretreatment with either 10-5 M 1-(β-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF96365) or 0.2 mM Ni2+ abolished the contraction induced by bradykinin in the presence of extracellular Ca2+. 4. Treatment with 10-5 M indomethacin completely inhibited the contractile response induced by Ca2+ replenishment, regardless of the timing of its application, before or after the application of bradykinin. 5. In endothelial cells in the valvular strips, bradykinin caused a transient [Ca2+]i elevation in the presence of 1.25 mM extracellular Ca2+, but [Ca2+]i returned to the resting level within 10 min. Neither 10-5 M SKF96365 nor 0.2mM Ni2+ had any effect on the peak [Ca2+]i elevation, but decreased [Ca2+]i in the declining phase. In the absence of extracellular Ca2+, bradykinin induced a transient [Ca2+]i elevation to a level similar to that seen in the presence of 1.25 mM extracellular Ca2+. However, [Ca2+]i then rapidly returned to the prestimulation level within 5 min. Subsequent Ca2+ replenishment to 0.75 mM and higher in the presence of bradykinin elevated [Ca2+]i to significantly higher levels than the resting level seen in the media containing 1.25 mM Ca2+. 6. In conclusion, Ca2+ influx in the endothelial cells is essential for bradykinin to induce endothelium-dependent contraction in the porcine interlobar renal artery.

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