Involvement of CGRP in the inhibitory effect of rutaecarpine on vasoconstriction induced by anaphylaxis in guinea pig

  title={Involvement of CGRP in the inhibitory effect of rutaecarpine on vasoconstriction induced by anaphylaxis in guinea pig},
  author={Jing Yu and Guishan Tan and Pan-Yue Deng and Kang-ping Xu and Chang-Ping Hu and Yuan‐jian Li},
  journal={Regulatory Peptides},

Involvement of TRPV1 in the expression and release of calcitonin gene-related peptide induced by rutaecarpine

It was concluded that TRPV1 was involved in the expression and release of CGRP stimulated by rutaecarpine, which provided novel mechanistic understanding of the treatment of hypertension using the Chinese herb Wu-Chu-Yu.

Rutaecarpine Induces Chloride Secretion across Rat Isolated Distal Colon

The evidence derived from present study suggests that Rut-stimulated Cl– secretion is mediated by generation of endogenous prostaglandin E2 and that it also involves the stimulation of cAMP and protein kinase A pathways, which subsequently lead to the activation of apical Cl– channels, mostly the CFTR and basolateral cAMP-dependent K+ channels.


The data suggest that the repression of increases in systolic blood pressure and reversal of mesenteric artery remodelling by rutaecarpine may be related to increased expression of PRCP in the circulation and small arteries in 2K1C hypertensive rats.

The protective effects of rutaecarpine on acute pancreatitis.

It is indicated that rutaecarpine protects against AP in rats by upregulating endogenous CGRP release via activation VR1 of, to improving the microcirculation of the pancreatic tissue and regulate the expression of inflammatory factors.

Low-Cytotoxic Synthetic Bromorutaecarpine Exhibits Anti-Inflammation and Activation of Transient Receptor Potential Vanilloid Type 1 Activities

The designed and synthesized a derivative of RUT, bromo-dimethoxyrutaecarpine (Br-RUT), which showed no cytotoxicity at 20 μM and retains its activities against inflammation and vasodilation that could be beneficial for cardiovascular disease therapeutics.

Solid dispersion of rutaecarpine improved its antihypertensive effect in spontaneously hypertensive rats

A change of the dosage from the crude drug to solid dispersion could improve significantly the efficiency of rutaecarpine absorption and increase its plasma concentration, and the anti‐hypertensive effect exerted by rutaECarpine solid disp immersion in SHR is mediated by CGRP.

Rutaecarpine prevents hypertensive cardiac hypertrophy involving the inhibition of Nox4‐ROS‐ADAM17 pathway

In vitro experiments confirmed the results of in vitro experiments that rutaecarpine significantly inhibited Ang II‐induced cardiac hypertrophy in primary cardiomyocytes and suppressed the Nox4‐ROS‐ADAM17 pathway and over‐activation of extracellular signal‐regulated kinase (ERK) 1/2 pathway in the left ventricle of AAC‐induced hypertensive rats and primary carduomyocytes stimulated with Ang II.

Pellitorine, an extract of Tetradium daniellii, is an antagonist of the ion channel TRPV1.

  • Z. OláhD. Rédei J. Hohmann
  • Biology, Chemistry
    Phytomedicine : international journal of phytotherapy and phytopharmacology
  • 2017

Anti-inflammatory and anti-infectious effects of Evodia rutaecarpa (Wuzhuyu) and its major bioactive components

Stimulation of calcitonin gene-related peptide release may partially explain the analgesic, cardiovascular and gastrointestinal protective, anti-obese activities of Evodia rutaecarpa and its major bioactive components.



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

The results suggest that the protective effects of rutaecarpine on cardiac anaphylactic injury are related to inhibition of TNF-alpha production by stimulation of CGRP release.

Release of calcitonin gene-related peptide in cardiac anaphylaxis

CGRP is not a primary mediator of the immediate hypersensitivity reaction of the heart, but is in turn released by arachidonic acid metabolites of the cyclooxygenase pathway and histamine, in contrast to LT, which obviously do not contribute to anaphylactic CGRP release.

On the mechanism of the protective effects of nitroglycerin and nicorandil in cardiac anaphylaxis

It is suggested that the protective effect of nitroglycerin may be related to stimulation of CGRP release and opening the KATP channel, and that the effect of nicorandil is mainly due to the activation of the K ATP channel.

The depressor and vasodilator effects of rutaecarpine are mediated by calcitonin gene-related peptide.

The results suggest that the depressor and vasodilator effects of rutaecarpine are related to stimulation of endogenous CGRP release via activation of vanilloid receptors in rats.

Protective effects of calcitonin gene-related peptide-mediated evodiamine on guinea-pig cardiac anaphylaxis

The results suggest that evodiamine possesses a protective effect of cardiac anaphylactic injury and that the effect of evodia rutaecarpa Bentham (Rutaceae) is related to stimulation of CGRP release.

Vasorelaxing action of rutaecarpine: effects of rutaecarpine on calcium channel activities in vascular endothelial and smooth muscle cells.

  • G. WangX. Wu P. Pang
  • Biology
    The Journal of pharmacology and experimental therapeutics
  • 1999
The results suggested that Rut lowered blood pressure by mainly activating the endothelial Ca2+-nitric oxide-cGMP pathway to reduce smooth muscle tone.

Inhibition of leukotriene release in anaphylactic guinea‐pig hearts by a 5‐lipoxygenase inhibitor, CGS 8515

It is concluded that leukotrienes have a major role in guinea‐pig cardiac anaphylaxis, and that CGS 8515 has a cardio‐protective action.

Endogenous vasodilators modulate pulmonary vascular anaphylaxis.

The response of guinea pig pulmonary arteries to antigen is modulated by two types of endogenous vasodilators, endothelium-derived nitric oxide that inhibits the initial phase of the response and an endothelia-independent relaxing factor that is guanosine 3',5'-cyclic monophosphate dependent and attenuates the duration of anaphylactic contraction.