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References in periodicals archive ?
The inhibition was significant at the second, third and fourth hours, when bradykinin is being released and there occurs an accumulation of prostaglandins and infiltration of polymorphonuclear cells.
procerum LAE, similarly to ASA, failed to interfere with the edematogenic response induced by bradykinin in the rat paw, a response independent of PGs (Teixeira et al.
The first phase is early mediated by mast cell degranulation and histamine and serotonin release (first h), the second phase (60 to 150 min) is characterized by bradykinin release and pain, and further eicosanoid production in the late phase (third-fourth h) (Di Rosa and Willoughby, 1971; Di Rosa, 1972; Goetzl, 1980).
In summary, we have demonstrated that bradykinin is heavily deposited in the stromal tissue and endothelial cells of a patient with erythema marginatum associated with hereditary angioedema.
However, unlike the impaired vasodilator response to bradykinin noted in hypertensive patients (33), the response to bradykinin in hypercholesterolemic subjects was found to be similar to the response of healthy subjects, suggestive of selective impairment of a G-protein-dependent pertussis toxin-sensitive signal transduction pathway in hypercholesterolemia (36).
In the light of these data, we may suggest that anti-inflammatory effects of CELS and MPE are mainly the result of mediating non-histaminergic pathways, which are mostly blocking the synthesis of serotonin, bradykinin, leukotrienes and/or polymorphonuclear cells.
By shifting the balance between angiotensin II and bradykinin, ACE inhibitors may modulate their various vascular effects (Fig.
It is well known that to investigate the effects of drugs on the acute phase of inflammation, models induced by pro-inflammatory agents such as carrageenan, dextrane, formaldehyde, serotonin, histamine and bradykinin in rat paws are employed (Campos et al.
The swelling seen in angioedema resembles what happens in patients with a C1 inhibitor deficiency, which is known to be caused by excess bradykinin production, said Harold J.
ACE inhibitors not only lower blood pressure, they also have antithrombotic properties, have antioxidant effects, potentiate bradykinin, reduce vascular inflammation, promote atherosclerotic plaque stabilization, reduce endothelial dysfunction, and curb deleterious vascular and cardiac remodeling.
The discovery of the important role of bradykinin in HAE has led to the development of icatibant, a synthetic peptide drug that selectively blocks the bradykinin receptor B2.
FIRAZYR's active substance, icatibant, is a potent and selective bradykinin B2 receptor antagonist.