Bronchoconstriction inhibition

Elevation of cycHc AMP levels is also known to inhibit the release of inflammatory and contractile mediators from mast cells (42). The good clinical efficacy of P2" goiAsts may be related to this action because some members of this class of dmgs inhibit mediator release at the same concentrations at which they relax smooth muscle (43). In contrast to their effectiveness against immediate bronchoconstriction, P2" gonists do not inhibit the late asthmatic... 

C22H23NNa202, (17), both inhibit the effect of sensory nerve activation, thereby interfering with bronchoconstriction (101). 

Adenosine is produced by many tissues, mainly as a byproduct of ATP breakdown. It is released from neurons, glia and other cells, possibly through the operation of the membrane transport system. Its rate of production varies with the functional state of the tissue and it may play a role as an autocrine or paracrine mediator (e.g. controlling blood flow). The uptake of adenosine is blocked by dipyridamole, which has vasodilatory effects. The effects of adenosine are mediated by a group of G protein-coupled receptors (the Gi/o-coupled Ai- and A3 receptors, and the Gs-coupled A2a-/A2B receptors). Ai receptors can mediate vasoconstriction, block of cardiac atrioventricular conduction and reduction of force of contraction, bronchoconstriction, and inhibition of neurotransmitter release. A2 receptors mediate vasodilatation and are involved in the stimulation of nociceptive afferent neurons. A3 receptors mediate the release of mediators from mast cells. Methylxanthines (e.g. caffeine) function as antagonists of Ai and A2 receptors. Adenosine itself is used to terminate supraventricular tachycardia by intravenous bolus injection. 

Leuko trienes are bronchoconstrictive substances released by the body during the inflammatory process. When leukotriene production is inhibited, bronchodilation is facilitated. Zileuton acts by decreasing tire formation of leukotrienes. Although the result is tire same, montelukast and zafirlukast work in a manner slightly differently from that of zileuton. Montelukast and zafirlukast are considered leukotriene receptor antagonists because they inhibit leukotriene receptor sites in the respiratory tract, preventing airway edema and facilitating bronchodilation. 

These dragp inhibit die release of substances that cause bronchoconstriction and inflammation from die mast cells in the respiratory tract. 

Respiratory Effects. Information on respiratory effects due to exposure to disulfoton is very limited. Exposure to disulfoton causes overstimulation of the muscarinic cholinergic receptors in the respiratory tract (Murphy 1986). This usually results in excessive bronchial secretions, bronchoconstriction, and eventually respiratory failure. Pulmonary edema and hemoptysis were recognized as probable causes of death in a man who ingested an unknown amount of disulfoton (Hattori et al. 1982). Studies regarding inhalation exposure were concerned primarily with lethality or cholinesterase inhibition. However, in intermediate-duration inhalation studies in rats, inflammation... 

Inhaled and intravenous histamine causes bronchoconstriction as one of the first recognized properties of histamine, which is inhibited by Hi antihistamines. As a manifestation of airway hyperresponsiveness, asthmatic individuals are more sensitive to the bronchoconstrictor effect of histamine than normal individuals. In addition, in vitro studies have shown increased histamine release in basophils and mast cells obtained from asthmatic subjects compared with... 

There are only a few reports on the efficacy of feverfew in an in vivo situation. Inhibition of collagen-induced bronchoconstriction in an in vivo guinea-pig model was demonstrated [56] and it was concluded that this was consistent with in vivo phospholipase A2 inhibition. In a rat model of experimentally induced nephrocalcinosis, parthenolide was shown to protect the rats against this condition. Inhibition of prostaglandin biosynthesis may have been the mechanism of action of parthenolide in this case, as prostaglandins are thought to be involved in nephrocalcinosis [57]. 

Beta-adrenoceptor blockers block the sympathetic system antagonising the effect on the lungs, resulting in bronchoconstriction. Non-steroidal anti-inflammatory drugs inhibit prostaglandin synthesis, which may lead to bronchoconstriction. 

Being an anticholinergic, ipratropium interrupts the parasympathetic activities including the blocking of muscarinic receptors in the lung, resulting in an inhibition of bronchoconstriction and of mucus secretion. 

Pharmacology Nedocromil is an inhaled anti-inflammatory agent for the preventive management of asthma. It inhibits the in vitro activation of, and mediator release from, a variety of inflammatory cell types associated with asthma, including eosinophils, neutrophils, macrophages, mast cells, monocytes and platelets. Nedocromil inhibits the development of early and late bronchoconstriction responses to inhaled antigen. 

Zileuton inhibits leukotriene-dependent smooth muscle contractions. Pretreatment with zileuton attenuated bronchoconstriction caused by cold air challenge in patients with asthma. 

Thromboxane A2 receptor TBXA2R Agonism Vaso-, bronchoconstriction. platelet aggregation, myocardial ischemia, heart failure. Antagonism could cause bleeding by inhibiting platelet aggregation. 

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