Asthma kinins

At the bronchi, predominantly /32-adrenoceptors are present on the smooth muscle cells. Therefor noradrenaline has hardly any influence on the muscular tonus whereas adrenaline induce a dilatation especially of precontracted bronchi, independent of the cause (histamine, acetylcholine, kinines, prostanoides). This effect can be used therapeutically in the therapy of bronchial asthma. In general the local application by aerosol is more useful than the systemic application, due to lesser side effects and the additional, beneficial effect of the reduction of mucosa swelling. 

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. 

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