English Journal

HOE-140, an antagonist of B2 receptor, protects against memory deficits and brain damage induced by moderate lateral fluid percussion injury in mice.

Ferreira AP1, Rodrigues FS, Della-Pace ID, Mota BC, Oliveira SM, de Campos Velho Gewehr C, Bobinski F, de Oliveira CV, Brum JS, Oliveira MS, Furian AF, de Barros CS, Dos Santos AR, Ferreira J, Fighera MR, Royes LF.Author information 1Laboratório de Bioquímica do Exercício, Departamento de Métodos e Técnicas Desportivas, Centro de Educação Física e Desportos, Universidade Federal de Santa Maria (UFSM), 97105-900, Santa Maria, RS, Brasil.AbstractRATIONALE: There are evidences indicating the role of kinins in pathophysiology of traumatic brain injury, but little is known about their action on memory deficits.
Psychopharmacology.Psychopharmacology (Berl).2013 Nov 8. [Epub ahead of print]
RATIONALE: There are evidences indicating the role of kinins in pathophysiology of traumatic brain injury, but little is known about their action on memory deficits.OBJECTIVES: Our aim was to establish the role of bradykinin receptors B1 (B1R) and B2 (B2R) on the behavioral, biochemical, and histolo
PMID 24202114

ACE inhibition enhances bradykinin relaxations through nitric oxide and B1 receptor activation in bovine coronary arteries.

Gauthier KM1, Cepura CJ, Campbell WB.Author information 1Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA. kgauth@mcw.eduAbstractBradykinin causes vascular relaxations through release of endothelial relaxing factors including prostacyclin, nitric oxide (NO) and epoxyeicosatrienoic acids (EETs). Bradykinin is metabolized by angiotensin converting enzyme (ACE) and ACE inhibition enhances bradykinin relaxations. Our goal was to characterize the role of bradykinin receptors and endothelial factors in ACE inhibitor-enhanced relaxations in bovine coronary arteries. In U46619 preconstricted arteries, bradykinin (10-11-10-8m) caused concentration-dependent relaxations (maximal relaxation ≥100%, log EC50=-9.8±0.1). In the presence of the NO synthase inhibitor, N-nitro-L-arginine (L-NA, 30 μm) and the cyclooxygenase inhibitor, indomethacin (10 μm), relaxations were reduced by an inhibitor of EET synthesis, miconazole (10 μm) (maximal relaxation=55±10%). Bradykinin relaxations were inhibited by the bradykinin 2 (B2) receptor antagonist, D-Arg0-Hyp3-Thi5,8-D-Phe7-bradykinin (1 μm) (log EC50=-8.5±0.1) but not altered by the B1 receptor antagonist, des-Arg9[Leu8]bradykinin (1 μm). Mass spectrometric analysis of bovine coronary artery bradykinin metabolites revealed a time-dependent increase in bradykinin (1-5) and (1-7) suggesting metabolism by ACE. ACE inhibition with captopril (50 μm) enhanced bradykinin relaxations (log EC50=-10.3±0.1). The enhanced relaxations were eliminated by L-NA or the B1 receptor antagonist but not the B2 receptor antagonist. Our results demonstrate that ACE inhibitor-enhanced bradykinin relaxations of bovine coronary arteries occur through endothelial cell B1 receptor activation and NO.
Biological chemistry.Biol Chem.2013 Sep;394(9):1205-12. doi: 10.1515/hsz-2012-0348.
Bradykinin causes vascular relaxations through release of endothelial relaxing factors including prostacyclin, nitric oxide (NO) and epoxyeicosatrienoic acids (EETs). Bradykinin is metabolized by angiotensin converting enzyme (ACE) and ACE inhibition enhances bradykinin relaxations. Our goal was to
PMID 23729620

Japanese Journal

The Enhancing Effects of Peptidase Inhibitors on the Antinociceptive Action of [Met5]Enkephalin-Arg6-Phe7 in Rats

Takahashi Shigeru,Jin Xing Lu,Kosaka Kenya,Yoshikawa Masanobu,Kobayashi Hiroyuki,Oka Tetsuo
Journal of Pharmacological Sciences 105(1), 117-121, 2007
… The present data, together with those obtained from previous studies, clearly show that amastatin-, captopril-, and phosphoramidon-sensitive enzymes play important roles in the inactivation of endogenous opioid peptides, such as [Met5]enkephalin, [Met5]enkephalin-Arg6-Phe7, [Met5]enkephalin-Arg6-Gly7-Leu8, and dynorphin A (1-8), administered intra-third-ventricularly to rats. …
NAID 130000075710

Different Prostanoids Are Involved in Bradykinin-Induced Endothelium-Dependent and-Independent Vasoconstriction in Rat Mesenteric Resistance Arteries

Nawa Hideki,Kurosaki Yuji,Kawasaki Hiromu
Journal of pharmacological sciences 94(2), 115-121, 2004-02-01
… these effects were abolished by FR172357 (bradykinin B2-receptor antagonist), but not by des-Arg9-[Leu8]-bradykinin (bradykinin B1-receptor antagonist). …
NAID 130000073862

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