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Enzymatic Degradation of Bradykinin
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Randal A. Skidgel, Ervin G. Erdös
Aminopeptidases can release Bk from kallidin (or Lys1-Bk) that is a product of tissue kallikrein, whereas Bk is liberated by plasma kallikrein (Bhoola et al., 1992). Early studies showed that Lys1-Bk is converted to Bk by an aminopeptidase in the blood, and subsequently, similar activity was detected in a variety of tissues (Erdös, 1979; Erdös et al., 1963; Webster and Pierce, 1963).
Sensory and Inflammatory Peptide Receptors in Airways
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
Bradykinin and related kinins are formed from plasma precursors as part of the inflammatory response. Bradykinin itself was first isolated in 1949 from enzymatic treatment of blood75 and later shown to be a nine-amino-acid peptide. Lysine-bradykinin (kallidin) has also been identified and has similar pharmacological properties.76
Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Plasma kininogens are glycoproteins with various molecular weights. Until now only two groups of kininogens have been identified.21,55,165,225,365 Low molecular weight (about 50,000 Da) kininogens I and II yield kallidin when treated with kallikrein isolated from human urine and bradykinin when treated with trypsin (Figure 11). High molecular weight kininogen A of about 200,000 Da, produces kallikrein when treated with urinary kallikrein, and bradykinin when treated with plasma kallikrein or trypsin. High molecular weight kininogen B is only affected by trypsin.
Kinin B1 receptors as a therapeutic target for inflammation
Published in Expert Opinion on Therapeutic Targets, 2018
Fatimunnisa Qadri, Michael Bader
One particularly important family of inflammatory mediators playing an integral role during inflammation is the kinins. Kinins are blood- and tissue-derived vasoactive hormones and consist mainly of the nonapeptide, bradykinin (BK, Arg–Pro–Pro–Gly–Phe–Ser–Pro–Phe–Arg), the decapeptide Lys-bradykinin or kallidin (KD), and their carboxy-terminal des-Arg metabolites, des-Arg9-BK (DABK) and des-Arg10-KD (DAKD), respectively. There are two classical pathways for the generation of kinins, the plasma and tissue kallikrein–kinin system (KKS) (Figure 1). Kinins originate from kininogens (high and low molecular weight), which are circulatory glycoproteins primarily synthetized by the liver. The cleavage of kininogens by the proteolytic enzymes, kallikreins, in either plasma or tissue produces the kinins, BK, and KD, respectively. Both BK and KD are highly instable peptides and can be degraded very fast by several kininases including angiotensin-converting enzyme (ACE), neutral endopeptidase (NEP), carboxypeptidase N (CPN), and carboxypeptidase M (CPM). These kininases are divided into two main types on the basis of their enzymology; kininase-I (CPN and CPM), and kininase-II (ACE). Kininase-I enzymes cleave the carboxyterminal arginine from either BK or KD giving rise to the active metabolites, DABK and DAKD, while the kininases-II cleave off the C-terminal dipeptide Phe–Arg [2–6].
Novel therapeutic agents for the treatment of diabetic kidney disease
Published in Expert Opinion on Investigational Drugs, 2020
Rachel E. Hartman, P.S.S. Rao, Mariann D. Churchwell, Susan J. Lewis
Tissue kallikrein is a serine protease which catalyzes the conversion of kininogen to bradykinin and kallidin in humans [150]. Bradykinin, via activation of bradykinin receptors (B1R and B2R), is known to induce nitric oxide production and vasodilation resulting in an anti-inflammatory and antiproliferative effect [151]. Intuitively, exogenous administration of kallikrein was found to have protective effects in a rodent model of DKD [152]. Based on its significance, the renal kallikrein-kinin system represents a unique target for treating DKD [153].
Influence of butyphthalide combined with urinary kallikrein in ACI treatment on neuro-cytokines and vascular endothelial function and its clinical effect
Published in International Journal of Neuroscience, 2021
Wenqin Zou, Yanqing Deng, Guanghui Chen, Shouqin Shangguan, Faming Zhou, Wenxin Jiang, Xiaoli Li
Acute cerebral infarction (ACI) is a disease of brain tissue necrosis which results from sudden interruption of blood supply for the brain. Usually, it is caused by cerebral atherosclerosis or thrombus. After cerebral atherosclerosis, vascular wall will become hard and fragile. Besides, hypertension and clotting mechanism abnormality also have certain influence. Finally, blood vessel of brain is blocked, thus leading to acute ischemia injury of local brain tissues, and the occurrence of long-term central nervous system sequelae [1]. Epidemiological investigation shows that the occurrence rate of ACI is 0.05 ∼ 0.11% [2,3]. Its clinical features mainly include headache, nausea, vomiting, tinnitus, sudden dizziness, and facial paralysis, and the final manifestations include symmetric paralysis and hemiplegia, etc. The severity of ACI is closely related to infraction position and range. Coma and even death happen to the severe cases [4–6]. At present, the clinical effect of ACI is limited, and the overall effective treatment rate is less than 35%. After treatment, the occurrence rate of long-term central nervous system complications is still high [7,8]. Butyphthalide as an anti-ischemic drug can obviously improve cerebral blood perfusion and promote repair of neurological functions. Urinary kallikrein can activate kininogenase-plasmakinin system, and it is a kind of human urinary kallikein. Besides, it can facilitate kininogen to be converted into kallidin, increase vasodilatin synthesis and release, selectively expand cerebral arteriole, improve blood oxygen supply of ischemic brain tissue and contribute to improving neurologic impairment function of ACI patients [9]. The influence of butyphthalide combined with urinary kallikrein in ACI treatment on neuro-cytokines, indicators of vascular endothelial function, CXCL16 and CD40L and its clinical effect were explored in this study.