Bronchial hyperresponsiveness is not bronchial hyperresponsiveness is not bronchial asthma.
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Acetylcholine↗
Biomedical subjects
G Joos
Publications and source records attributed to G Joos.
Effect of inhaled substance P and neurokinin A on the airways of normal and asthmatic subjects.
The neuropeptides substance P and neurokinin A are present in sensory airway nerves. Their effect on airway calibre was compared in six healthy non-smoking subjects and six asthmatic subjects. On separate days increasing concentrations (from 10(-9) to 10(-6) mol/ml) of each neuropeptide were administered by nebuliser and the airway response measured as change in specific airway conductance (sGaw). Substance P and neurokinin A caused no change in sGaw in the healthy subjects. Inhalation of substance P up to the highest concentration of 10(-6) mol/ml caused no change in sGaw in the asthmatic subjects. Neurokinin A, however, caused bronchoconstriction with a mean fall in sGaw of 48% (SEM 12%) after 5 x 10(-7) mol/ml. The onset of bronchoconstriction was rapid, but sGaw had returned to baseline values within one hour in all but one patient.
Administration, Inhalation↗
The effect of tachykinins on the conducting airways of the rat.
We studied the bronchial effects of intravenously administered tachykinins in inbred rats. Substance P and related tachykinins caused a dose-dependent bronchoconstriction. The bronchial reactivity to substance P differed significantly between different inbred rat strains. Substance K, eledoisin and kassinin were more potent than substance P in causing bronchoconstriction. This suggests a predominance in the bronchi of SP-E receptors. The bronchial effects of substance P and eledoisin were largely inhibited by atropine and slightly enhanced by hexamethonium. In addition to a direct effect on airway smooth muscle, tachykinins interfere with the cholinergic airway innervation of the rat at the ganglionic and postganglionic level.
Airway Resistance↗
The respiratory effects of neuropeptides.
Several peptides have been localised to pulmonary nerves and endocrine cells. The neuropeptides vasoactive intestinal polypeptide (VIP) and substance P have potent effects on the airway smooth muscle, bronchial glands and blood vessels. There is increasing evidence that VIP and substance P are neurotransmitters of the non-adrenergic, non-cholinergic nervous (NANC) system. Non-adrenergic inhibitory nerves are the predominant inhibitory nervous system of the human airways. The presence of VIP in the innervation of the airways and the demonstration that it can mimick the effect of NANC nerve stimulation supports the hypothesis that it could be a mediator of the NANC system in the lungs. Sensory nerve fibers containing substance P can contribute to the smooth muscle contraction and mucosal oedema seen in asthma, by local axon reflexes that are initiated by noxious stimuli, such as for example cigarette smoke. A rat model for study of the bronchial reaction to substance P and related tachykinins, is described. In addition to a direct effect on airway smooth muscle, a large part of the broncho-constrictory actions of tachykinins in the rat is mediated by interaction with cholinergic nerves.
Airway Resistance↗
Cor pulmonale and respiratory failure in a young woman.
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Adult↗
Synergistic mechanisms in the adenosine- and neuropeptide-induced bronchoconstriction.
Neuropeptides and purines are possible neurotransmitters of the nonadrenergic noncholinergic nervous system of the airways. We investigated possible synergistic mechanisms between these two bronchoconstricting agents in a rat model. We observed that both adenosine and tachykinins enhance histamine release in the airways and that adenosine and neurokinin A act synergistically both on airway narrowing and histamine release.
Acetylcholine↗