Changes in components of the kinin system and structure of myocardium caused by antikinin preparations in rabbits with allergic myocarditis

1976 ◽  
Vol 82 (2) ◽  
pp. 1225-1227 ◽  
Author(s):  
M. S. Surovikina ◽  
V. A. Odinokova ◽  
N. R. Paleev ◽  
M. A. Gurevich ◽  
M. O. Yankovskaya
Keyword(s):  
Kinin System ◽  
Allergic Myocarditis

Einfluss mechanischer Dehnung von alveolären Typ II Zellen auf das Kallikrein-Kinin System

Pneumologie ◽  
2016 ◽  
Vol 70 (S 01) ◽  
Author(s):  
J Knauth ◽  
A Schweinberger ◽  
H Kuhn ◽  
H Wirtz
Keyword(s):  
Kinin System ◽  
Kallikrein Kinin System

scholarly journals A Systematic Review of Molecular Imaging Agents Targeting Bradykinin B1 and B2 Receptors

2020 ◽  
Vol 13 (8) ◽  
pp. 199
Author(s):  
Joseph Lau ◽  
Julie Rousseau ◽  
Daniel Kwon ◽  
François Bénard ◽  
Kuo-Shyan Lin
Keyword(s):  
Molecular Imaging ◽  
Smooth Muscle Contraction ◽  
Therapeutic Interventions ◽  
Imaging Agents ◽  
Kinin System ◽  
Normal Tissues ◽  
Molecular Imaging Agents ◽  
Inflammatory State ◽  
B2 Receptors ◽  
Tissue Trauma

Kinins, bradykinin and kallidin are vasoactive peptides that signal through the bradykinin B1 and B2 receptors (B1R and B2R). B2R is constitutively expressed in healthy tissues and mediates responses such as vasodilation, fluid balance and retention, smooth muscle contraction, and algesia, while B1R is absent in normal tissues and is induced by tissue trauma or inflammation. B2R is activated by kinins, while B1R is activated by kinins that lack the C-terminal arginine residue. Perturbations of the kinin system have been implicated in inflammation, chronic pain, vasculopathy, neuropathy, obesity, diabetes, and cancer. In general, excess activation and signaling of the kinin system lead to a pro-inflammatory state. Depending on the disease context, agonism or antagonism of the bradykinin receptors have been considered as therapeutic options. In this review, we summarize molecular imaging agents targeting these G protein-coupled receptors, including optical and radioactive probes that have been used to interrogate B1R/B2R expression at the cellular and anatomical levels, respectively. Several of these preclinical agents, described herein, have the potential to guide therapeutic interventions for these receptors.

scholarly journals Kinins and Kinin Receptors in Cardiovascular and Renal Diseases

2021 ◽  
Vol 14 (3) ◽  
pp. 240
Author(s):  
Jean-Pierre Girolami ◽  
Nadine Bouby ◽  
Christine Richer-Giudicelli ◽  
Francois Alhenc-Gelas
Keyword(s):  
Experimental Studies ◽  
Physiological Role ◽  
Renal Diseases ◽  
Kinin System ◽  
Genetic Studies ◽  
Pharmacological Manipulation ◽  
Kininase Ii ◽  
Kinin Receptors ◽  
Kallikrein Kinin System

This review addresses the physiological role of the kallikrein–kinin system in arteries, heart and kidney and the consequences of kallikrein and kinin actions in diseases affecting these organs, especially ischemic and diabetic diseases. Emphasis is put on pharmacological and genetic studies targeting kallikrein; ACE/kininase II; and the two kinin receptors, B1 (B1R) and B2 (B2R), distinguished through the work of Domenico Regoli and his collaborators. Potential therapeutic interest and limitations of the pharmacological manipulation of B1R or B2R activity in cardiovascular and renal diseases are discussed. This discussion addresses either the activation or inhibition of these receptors, based on recent clinical and experimental studies.

scholarly journals Haplotype-based association study between PRCP gene polymorphisms and essential hypertension in Hani minority group from a remote region of China

2020 ◽  
Vol 21 (4) ◽  
pp. 147032032098131
Author(s):  
Yanrui Wu ◽  
Xingming Pan ◽  
Xiaoxiao Jin
Keyword(s):  
Essential Hypertension ◽  
Gene Polymorphisms ◽  
Minority Group ◽  
Normal Subjects ◽  
Nucleotide Polymorphisms ◽  
Remote Region ◽  
Kinin System ◽  
Average Blood Pressure ◽  
Genetic Impact ◽  
Kallikrein Kinin System

Objective: Prolylcarboxypeptidase (PRCP) is both involved in the Kallikrein-Kinin system (KKS) and renin-angiotensin-aldosterone system (RAAS). This study aimed to determine the genetic impact of PRCP gene polymorphisms on essential hypertension (EH) in an isolated population from a remote region of China. Methods: A haplotype-based study was investigated in 346 EH patients and 346 normal subjects and all samples were Hani minority residents in Southwest China. A total of 11 tag single nucleotide polymorphisms (SNPs) in PRCP gene were tested by polymerase chain reaction-restriction fragment length polymorphism method. Results: Single site analysis found that PRCP gene 3′UTR SNP rs3750931 was associated with EH. The minor allele G of rs3750931 was more prevalent in the EH patients compared to control subjects after Bonferroni correction ( p < 0.05). Moreover, the rs3750931 G allele carriers showed higher average blood pressure (BP) level among the subjects. The H2 (GAGCACTAACA) haplotype without rs3750931 G allele showed the protective effect for EH (OR = 0.68, 95 CI 0.54–0.85, p = 0.001). Conclusion: The present study indicated PRCP gene rs3750931 was associated with the risk of EH. This SNP G allele could be considered as one of risk markers for EH in Hani population.

scholarly journals Kinin B2 Receptor Activation Prevents the Evolution of Alzheimer’s Disease Pathological Characteristics in a Transgenic Mouse Model

2020 ◽  
Vol 13 (10) ◽  
pp. 288
Author(s):  
Marielza Andrade Nunes ◽  
Mariana Toricelli ◽  
Natalia Mendes Schöwe ◽  
Helena Nascimento Malerba ◽  
Karis Ester Dong-Creste ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Functional Disability ◽  
Therapeutic Option ◽  
Receptor Activation ◽  
Hippocampal Culture ◽  
Kinin System ◽  
Organotypic Hippocampal Culture ◽  
Kallikrein Kinin System

Background: Alzheimer’s disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even death. Our group has demonstrated changes in the kallikrein–kinin system (KKS) in Alzheimer’s disease (AD) experimental models, but there is a lack of evidence about the role of the KKS in Alzheimer’s disease. Aim: In order to answer this question, we evaluated the potential of the kinin B2 receptors (BKB2R) to modify AD characteristics, particularly memory impairment, neurodegeneration, and Aβ peptide deposition. Methods: To assess the effects of B2, we used transgenic Alzheimer’s disease mice treated with B2 receptor (B2R) agonists and antagonists, and performed behavioral and biochemical tests. In addition, we performed organotypic hippocampal culture of wild-type (WT) and transgenic (TG) animals, where the density of cytokines, neurotrophin BDNF, activated astrocyte marker S100B, and cell death were analyzed after treatments. Results: Treatment with the B2R agonist preserved the spatial memory of transgenic mice and decreased amyloid plaque deposition. In organotypic hippocampal culture, treatment with B2R agonist decreased cell death, neuroinflammation, and S100B levels, and increased BDNF release. Conclusions: Our results indicate that the kallikrein–kinin system plays a beneficial role in Alzheimer’s disease through B2R activation. The use of B2R agonists could, therefore, be a possible therapeutic option for patients diagnosed with Alzheimer’s disease.

Sign in / Sign up

Export Citation Format

Share Document