Protective effects of rutaecarpine in cardiac anaphylactic injury is mediated by CGRP

Hong Hui Yi; Wei Qing Rang; Pan Yue Deng; Chang Ping Hu; Gui Zhen Liu; Gui Shan Tan; Kang Ping Xu; Yuan Jian Li

doi:10.1055/s-2004-835840

Protective effects of rutaecarpine in cardiac anaphylactic injury is mediated by CGRP

Hong Hui Yi, Wei Qing Rang, Pan Yue Deng, Chang Ping Hu, Gui Zhen Liu, Gui Shan Tan, Kang Ping Xu, Yuan Jian Li

Department of Cell Biology & Physiology

Research output: Contribution to journal › Article › peer-review

23 Scopus citations

Abstract

Previous investigations have indicated that rutaecarpine activates the vanilloid receptor to evoke calcitonin gene-related peptide (CGRP) release. CGRP has been shown to alleviate cardiac anaphylactic injury. In the present study, the effect of rutaecarpine on cardiac anaphylaxis was examined. Challenge of presensitized guinea-pig hearts with a specific antigen caused marked decreases in coronary flow (CF), left ventricular pressure (LVP) and its derivatives (± dp/dt_max), an increase in heart rate, and prolongation of the P-R interval. Rutaecarpine (0.3 or 1 μM) markedly increased the content of calcitonin gene-related peptide (CGRP) in the coronary effluent and decreased the content of tumor necrosis factor-α (TNF-α) in myocardial tissues concomitantly with a significant improvement of cardiac function and alleviation of the extension of the P-R interval. Rutaecarpine at the concentration of 1 μM also inhibited the sinus tachycardia. The protective effects of rutaecarpine on cardiac anaphylaxis were abolished by CGRP _8-37, a selective CGRP receptor antagonist. These results suggest that the protective effects of rutaecarpine on cardiac anaphylactic injury are related to inhibition of TNF-α production by stimulation of CGRP release.

Original language	English
Pages (from-to)	1135-1139
Number of pages	5
Journal	Planta Medica
Volume	70
Issue number	12
DOIs	https://doi.org/10.1055/s-2004-835840
State	Published - Dec 2004

Keywords

Calcitonin gene-related peptide (CGRP)
Cardiac anaphylaxis
Guinea-pig
Rutaecarpine
Tumor necrosis factor-α (TNF-α)

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title = "Protective effects of rutaecarpine in cardiac anaphylactic injury is mediated by CGRP",

abstract = "Previous investigations have indicated that rutaecarpine activates the vanilloid receptor to evoke calcitonin gene-related peptide (CGRP) release. CGRP has been shown to alleviate cardiac anaphylactic injury. In the present study, the effect of rutaecarpine on cardiac anaphylaxis was examined. Challenge of presensitized guinea-pig hearts with a specific antigen caused marked decreases in coronary flow (CF), left ventricular pressure (LVP) and its derivatives (± dp/dtmax), an increase in heart rate, and prolongation of the P-R interval. Rutaecarpine (0.3 or 1 μM) markedly increased the content of calcitonin gene-related peptide (CGRP) in the coronary effluent and decreased the content of tumor necrosis factor-α (TNF-α) in myocardial tissues concomitantly with a significant improvement of cardiac function and alleviation of the extension of the P-R interval. Rutaecarpine at the concentration of 1 μM also inhibited the sinus tachycardia. The protective effects of rutaecarpine on cardiac anaphylaxis were abolished by CGRP 8-37, a selective CGRP receptor antagonist. These results suggest that the protective effects of rutaecarpine on cardiac anaphylactic injury are related to inhibition of TNF-α production by stimulation of CGRP release.",

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author = "Yi, {Hong Hui} and Rang, {Wei Qing} and Deng, {Pan Yue} and Hu, {Chang Ping} and Liu, {Gui Zhen} and Tan, {Gui Shan} and Xu, {Kang Ping} and Li, {Yuan Jian}",

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AU - Yi, Hong Hui

AU - Rang, Wei Qing

AU - Deng, Pan Yue

AU - Hu, Chang Ping

AU - Liu, Gui Zhen

AU - Tan, Gui Shan

AU - Xu, Kang Ping

AU - Li, Yuan Jian

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N2 - Previous investigations have indicated that rutaecarpine activates the vanilloid receptor to evoke calcitonin gene-related peptide (CGRP) release. CGRP has been shown to alleviate cardiac anaphylactic injury. In the present study, the effect of rutaecarpine on cardiac anaphylaxis was examined. Challenge of presensitized guinea-pig hearts with a specific antigen caused marked decreases in coronary flow (CF), left ventricular pressure (LVP) and its derivatives (± dp/dtmax), an increase in heart rate, and prolongation of the P-R interval. Rutaecarpine (0.3 or 1 μM) markedly increased the content of calcitonin gene-related peptide (CGRP) in the coronary effluent and decreased the content of tumor necrosis factor-α (TNF-α) in myocardial tissues concomitantly with a significant improvement of cardiac function and alleviation of the extension of the P-R interval. Rutaecarpine at the concentration of 1 μM also inhibited the sinus tachycardia. The protective effects of rutaecarpine on cardiac anaphylaxis were abolished by CGRP 8-37, a selective CGRP receptor antagonist. These results suggest that the protective effects of rutaecarpine on cardiac anaphylactic injury are related to inhibition of TNF-α production by stimulation of CGRP release.

AB - Previous investigations have indicated that rutaecarpine activates the vanilloid receptor to evoke calcitonin gene-related peptide (CGRP) release. CGRP has been shown to alleviate cardiac anaphylactic injury. In the present study, the effect of rutaecarpine on cardiac anaphylaxis was examined. Challenge of presensitized guinea-pig hearts with a specific antigen caused marked decreases in coronary flow (CF), left ventricular pressure (LVP) and its derivatives (± dp/dtmax), an increase in heart rate, and prolongation of the P-R interval. Rutaecarpine (0.3 or 1 μM) markedly increased the content of calcitonin gene-related peptide (CGRP) in the coronary effluent and decreased the content of tumor necrosis factor-α (TNF-α) in myocardial tissues concomitantly with a significant improvement of cardiac function and alleviation of the extension of the P-R interval. Rutaecarpine at the concentration of 1 μM also inhibited the sinus tachycardia. The protective effects of rutaecarpine on cardiac anaphylaxis were abolished by CGRP 8-37, a selective CGRP receptor antagonist. These results suggest that the protective effects of rutaecarpine on cardiac anaphylactic injury are related to inhibition of TNF-α production by stimulation of CGRP release.

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Protective effects of rutaecarpine in cardiac anaphylactic injury is mediated by CGRP

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