Bradykinin induces vascular contraction after hemorrhagic shock in rats

Zhang, Jie; Yang, Guangming; Zhu, Yu; Peng, Xiaoyong; Liu, Liangming; Li, Tao

doi:10.1016/j.jss.2014.06.033

Cited by 9 publications

(8 citation statements)

References 32 publications

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“…Alonso et al (4) showed that Cx43 is increased in renin-dependent hypertension via ANG II activation of extracellular signal-regulated kinase and NF-B pathways. Our previous study demonstrated that Cx43 takes part in the regulation of vascular contractile responses after shock and that Rock1 has an important mediating effect in this process (35,66). The present study showed that Cx43 takes part in the regulation of vascular permeability in vital organs, such as the lungs, kidneys, and mesentery during sepsis, and that Rock1-MLC 20 phosphorylation is the main signaling pathway in this process.…”

Section: Discussionsupporting

confidence: 54%

“…Aslam et al (6) reported that activation of the RhoA/Rock pathway by thrombin induces VHP. We previously showed (32,66) that the regulation of vascular reactivity by Cx43 is related to the RhoA/Rock-MLC 20 pathway after shock. Hence, we hypothesized that Cx43 may participate in the regulation of vascular permeability and that the mechanism may be closely related to the Rock-MLC 20 pathway.…”

mentioning

confidence: 99%

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Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Zhang

Yang

Zhu

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC20 pathway in septic rats. Am J Physiol Lung Cell Mol Physiol 309: L1323-L1332, 2015. First published September 4, 2015 doi:10.1152/ajplung.00016.201543 has been shown to participate in several cardiovascular diseases. Increased vascular permeability is a common and severe complication in sepsis or septic shock. Whether or not Cx43 takes part in the regulation of vascular permeability in severe sepsis is not known, and the underlying mechanism has not been described. With cecal ligation and puncture-induced sepsis in rats and lipopolysaccharide (LPS)-treated vascular endothelial cells (VECs) from pulmonary veins, the role of Cx43 in increased vascular permeability and its relationship to the RhoA/Rock1 pathway were studied. It was shown that vascular permeability in the lungs, kidneys, and mesentery in sepsis rats and LPS-stimulated monolayer pulmonary vein VECs was significantly increased and positively correlated with the increased expression of Cx43 and Rock1 in these organs and cultured pulmonary vein VECs. The connexin inhibitor carbenoxolone (10 mg/kg iv) and the Rock1 inhibitor Y-27632 (2 mg/kg iv) alleviated the vascular leakage of lung, mesentery, and kidney in sepsis rats. Overexpressed Cx43 increased the phosphorylation of 20-kDa myosin light chain (MLC 20) and the expression of Rock1 and increased the vascular permeability and decreased the transendothelial electrical resistance of pulmonary vein VECs. Cx43 RNA interference decreased the phosphorylation of MLC20 and the expression of Rock1 and decreased LPS-stimulated hyperpermeability of cultured pulmonary vein VECs. The Rock1 inhibitor Y-27632 alleviated LPS-and overexpressed Cx43-induced hyperpermeability of monolayer pulmonary vein VECs. This report shows that Cx43 participates in the regulation of vascular permeability in sepsis and that the mechanism is related to the Rock1-MLC20 phosphorylation pathway. connexin 43; vascular permeability; sepsis; RhoA/Rock1 pathway; MLC 20

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Section: Discussionsupporting

confidence: 54%

mentioning

confidence: 99%

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Zhang

Yang

Zhu

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…For instance, in the 1960s, a secondary hypertensive response to bradykinin was described in both nephrectomized and pentolinium-treated rats (Croxatto & Belmar, 1961), as well as in anaesthetized cats and dogs (Lang & Pearson, 1968;Pearson & Lang, 1967). This pressor response to bradykinin was characterized as more intense under drug-or haemorrhage-induced hypotension and was assigned to activation of the sympathetic nervous system, a peripheral release of catecholamines (Croxatto & Belmar, 1961;Lang & Pearson, 1968) and an unexplored activation of Rho-associated kinase (ROCK; Zhang et al, 2015). In our experiments, bradykinin-increased BP was not accompanied by any rise in the cardiac frequency, and it was not blocked by the α 1 -adrenoceptor antagonist prazosin.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin increases BP in endotoxemic rat: functional and biochemical evidence of angiotensin II AT₁/bradykinin B₂ receptor heterodimerization

Anton

Fernandes

Assreuy

et al. 2019

British J Pharmacology

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Background and Purpose Bradykinin may induce vasoconstriction in selected vessels or under specific experimental conditions. We hypothesized that inflammatory stimuli, such as endotoxin challenge, may induce the dimerization of AT1/B2 receptors, altering the vascular effects of bradykinin. Experimental Approach Wistar rats received LPS (1 mg·kg−1, i.p.) and were anaesthetized for assessment of BP. Mesenteric resistance arteries were used in organ baths and subjected to co‐immunoprecipitation and Western blot analyses. Key Results At 24 and 48 hr after LPS, bradykinin‐induced hypotension was followed by a sustained increase in BP, which was not found in non‐endotoxemic animals. The B2 receptor antagonist Hoe‐140 fully blocked the responses to bradykinin. The pressor effect of bradykinin was not prevented by prazosin, an α1‐adrenoceptor antagonist, but it was inhibited by the AT1 receptor antagonist losartan or the Rho‐kinase inhibitor Y‐27632. Endotoxemic rats also displayed enhanced pressor responses to angiotensin II, which were blocked by Hoe‐140. Co‐immunoprecipitation isolated using anti‐B2 or anti‐AT1 receptor antibodies showed that resistance arteries presented augmented levels of the AT1/B2 receptor complexes at 24 hr after LPS injection. The presence of AT1/B2 receptor heterodimers did correlate with the development of losartan‐sensitive contractile responses to bradykinin and potentiation of angiotensin II‐induced contraction, which was prevented by Hoe‐140. Conclusions and Implications Endotoxin challenge is a stimulus for AT1/B2 receptor heterodimerization in native vessels and shifts the B2 receptor‐dependent vascular effect of bradykinin to a more complex pathway, which also depends on AT1 receptors and their intracellular signalling pathways.

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“…Відповідно ми вивчали вплив похідних 3-заміщених 1,4-бенздіазепінонів на скоротливі відповіді препаратів ГМ шлунку щурів у випадку активації проведення збуджуючого сигналу шляхами фармакомеханічного спряження збудження-скорочення. Але початково виникла потреба розглянути особливості дії брадикініну та його конкурентного інгібітора на гладенькі м'язи шлунку, оскільки в літературі описаний вплив даного пептиду на м'язовий тонус уретри [7], кровоносних судин [3,5,12], тоді як його дія на шлунок не відома. На рис.1 (крива 1) наведено лінеаризацію механограм першої фази скорочень викликаних брадикініном в концентраціях від 10 -10 до 10 -5 М. При цьому нормована максимальна швидкість скорочення V n приймала значення від 5,25±0,21 (r = 0,98 -0,99) при 10 -10 М до 3,74±0,13 при 10 -5 М, зберігаючи лінійність.…”

Section: результати та обговоренняunclassified

“…Дія МСМ порушує транспорт амінокислот, спричиняє перекисне окиснення ліпідів (ПОЛ) у тканинах мозку. Зростання рівня МСМ у 3-5 і більше разів впливає на процеси метаболізму, мембранного транспорту речовин, клітинний імунітет, фагоцитоз, гліколіз, глюконеогенез, еритропоез, тканинне дихання, мікроциркуляцію, лімфодинаміку, синтез нуклеїнових кислот, цитопротекцію, процеси антикоагуляції тощо [3].…”

Section: Features Bradykinin-induced Smooth Muscle Contraction Of Stounclassified

Features of the bradykinin-induced contraction of the gastric smooth muscle depending on the concentration of compounds based on 3-substituted-1,4-benzodiazepin-2-ones

2016

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П. Вірич, асп., О. Шелюк, канд. біол. наук, В. Мартинюк, д-р біол. наук Київський національний університет імені Тараса Шевченка, Київ, В. Павловський, д-р хім. наук Фізико-хімічний інститут імені О.В. Богатського НАН України, Одеса ОСОБЛИВОСТІ БРАДИКІНІН-ІНДУКОВАНОГО СКОРОЧЕННЯ ГЛАДЕНЬКИХ М'ЯЗІВ ШЛУНКУ ЗАЛЕЖНО ВІД КОНЦЕНТРАЦІЇ СПОЛУК НА ОСНОВІ 3-ЗАМІЩЕНИХ 1,4-БЕНЗДІАЗЕПІН-2-ОНІВ Досліджено вплив сполук на основі 3-заміщених-1,4-бензидіазепін-2-онів на скоротливу активність гладеньких м'язів шлунку щурів. Дія речовин МХ-1626, МХ-1775 схожа за патернами скорочення з конкурентними інгібітором брадикініну -des-Arg9-[Leu8]-Bradykinin acetate, що спостерігається у вигляді зростання нормованої швидкості скорочення по мірі зростання кількості брадикініну і характеризується помітним сповільненням першої фази скорочення. Найбільш ефективними 3-заміені 1,4-бенздіазепін-2-они виявились за низьких концентрацій брадикініну, при збільшенні якого їх дія зменшується. Ключові слова: гладенькі м'язи, механокінетичні параметри, 3-заміщені 1,4-бенздіазепін-2-они. Список використаних джерел.

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Bradykinin induces vascular contraction after hemorrhagic shock in rats

Cited by 9 publications

References 32 publications

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Bradykinin increases BP in endotoxemic rat: functional and biochemical evidence of angiotensin II AT₁/bradykinin B₂ receptor heterodimerization

Features of the bradykinin-induced contraction of the gastric smooth muscle depending on the concentration of compounds based on 3-substituted-1,4-benzodiazepin-2-ones

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Bradykinin induces vascular contraction after hemorrhagic shock in rats

Cited by 9 publications

References 32 publications

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC20pathway in septic rats

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC20pathway in septic rats

Bradykinin increases BP in endotoxemic rat: functional and biochemical evidence of angiotensin II AT1/bradykinin B2 receptor heterodimerization

Features of the bradykinin-induced contraction of the gastric smooth muscle depending on the concentration of compounds based on 3-substituted-1,4-benzodiazepin-2-ones

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Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Bradykinin increases BP in endotoxemic rat: functional and biochemical evidence of angiotensin II AT₁/bradykinin B₂ receptor heterodimerization