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Soybean-Based Functional Foods Through Microbial Fermentation: Processing and Biological Activities
Published in Megh R. Goyal, Arijit Nath, Rasul Hafiz Ansar Suleria, Plant-Based Functional Foods and Phytochemicals, 2021
Arijit Nath, Titas Ghosh, Abinit Saha, Klára Pásztorné Huszár, Szilvia Bánvölgyi, Renáta Gerencsérné Berta, Ildikó Galambos, Edit Márki, Gyula Vatai, Andras Koris, Arpita Das
Due to presence of an angiotensin-converting enzyme (ACE) in soybean products, Angiotensin-I is converted to Angiotensin-II in the rennin-angio-tensin pathway, which promotes vasoconstriction and high blood pressure (BP). Also, ACE supports the transformation of bradykinin into inactive metabolites [17].
Drug Allergy
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Urticaria and angioedema are the most common IgE-mediated manifestations though they can occur with non IgE reactions such as serum sickness. Angioedema due to ACE inhibitors is mediated by bradykinin.
Proinflammatory Peptides in Relation to Other Inflammatory Mediators
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Pierangelo Geppetti, Costanza Emanueli, Michela Figini, Domenico Regoli
Bradykinin is a pleiotropic molecule that interacts with a variety of cells, producing a broad series of biological responses. Inflammatory responses to bradykinin may be mediated by direct activation of bradykinin receptors, usually of the B2 type, on effector cells. However, in-vivo conditions and particularly when bradykinin is administered locally, direct contribution of kinin receptor activation on effector cells is minor, whereas the ability of bradykinin to release different mediators that orchestrate a complex biological response is more evident. Recent studies have also shown that bradykinin may release mediators that exert antiinflammatory action. Thus, the final response to bradykinin reflects the contrasting actions of the different mediators released by this autacoid. One example of these possible interactions is the bronchoconstriction induced by bradykinin in guinea pigs. Bradykinin, if injected intravenously, causes a bronchoconstrictor response that is mediated by prostanoids, and in minor part by an atropine-sensitive cholinergic reflex pathway. If is administered by aerosolization, the constrictor effect of bradykinin is mediated mainly by tachykinin release from sensory nerve endings (57), although in this case also, a minor contribution of cholinergic nerves has been described (57).
Pharmacological approaches to treat intestinal pain
Published in Expert Review of Clinical Pharmacology, 2023
Mikolaj Swierczynski, Adam Makaro, Agata Grochowska, Maciej Salaga
In contrast to CB1, CB2 is predominantly expressed in immune cells and tissues. In the intestine, CB2 plays a key role in immune homeostasis since it is primarily found in macrophages [114,119]. However, it was showed that the activation of CB2 induces intestinal analgesia through modulation of the mesenteric afferent nerves. The use of synthetic CB2 agonist prevented mice from pain responses to bradykinin. Anti-nociceptive properties of the tested substance were not apparent in animals simultaneously exposed to synthetic CB2 antagonist as well as in CB2 knockout mice [120]. In another study, oral administration of Lactobacillus acidophilus increased the expression of CB2 and MOR in rodential colonic tissues through an unknown mechanism. The therapy with probiotic resulted in increased pain threshold, which was not observed in rats treated with i.p. administered CB2 antagonist [121]. Human studies evaluated the use of peripherally restricted and selective CB2 agonist on visceral pain. This drug, olorinab, reduced abdominal pain scores in CD patients. A similar effect of olorinab was observed in IBS-C patients with initially moderate-to-severe pain [122].
Severe Heloderma spp. envenomation: a review of the literature
Published in Clinical Toxicology, 2021
Jean-Philippe Chippaux, Karim Amri
In humans, severe pain, in addition to the trauma of a prolonged bite, and hypotension result from the physiological effects of horridum toxin, helodermatin and gilatoxin which release bradykinin and angiotensins I and II [28,31–34]. Helodermatin also releases bradykinin, a potent vasodilator that causes a sudden drop in blood pressure, but does not degrade either fibrinogen or plasminogen [32]. The high and abrupt release of bradykinin could explain angioedema, the etiology of which remains unclear, especially since respiratory tract angioedema and vasoplegic shock are generally not associated with other allergic symptoms, especially skin symptoms (pruritus, urticaria, rash, etc.). This suggests non-allergic bradykinin angioedema rather than helodermatid venom anaphylaxis [35], as already suggested [10,29]. However, to our knowledge, immunoglobulins E were never assayed.
Plasma concentrations of tissue kallikrein in normal and preeclamptic pregnancies
Published in Hypertension in Pregnancy, 2020
Chunyan Yuan, Yuyu Yao, Cong Fu, Tianai Rong, Bing Li, Abdlay Carvalho, Chang Liu
Tissue kallikrein (TK) is a serine protease that converts kininogen to the vasoactive peptides bradykinin (3). Bradykinin is a potent vasodilator that plays important roles in controlling vascular tone, local blood flow, electrolyte and glucose transport, pain, inflammation, and vascular permeability (4). The kallikrein-kinin system has a significant role in the regulation of systemic blood pressure (5). Transgenic mice carrying the human TK gene had significantly lower blood pressure (6). TK is significantly reduced in the urine of patients with essential hypertension (7). In addition, clinical studies have shown that the blood pressure of hypertensive patients can be temporarily lowered by oral administration of porcine pancreatic kallikrein (8). These results suggest that TK is involved in blood pressure homeostasis.