Effects of neurotransmitters on tracheobronchial blood flow.

Blood flow in the tracheobronchial airways is regulated by three main nervous pathways: 1) sympathetic motor nerves (adrenergic and nonadrenergic); 2) parasympathetic motor nerves (cholinergic and noncholinergic); and 3) afferent or sensory nerves (peptidergic). Noradrenaline is the main adrenergic mediator which produces short-lasting constrictions in both tracheal and bronchial vascular beds and in both arteries and veins. These responses are mediated via alpha-adrenoceptors. The nonadrenergic mediator neuropeptide Y is a vasoconstrictor which produces long-lasting responses with larger doses. Acetylcholine is the principal mediator of the cholinergic nerves and causes short-lasting dilations at all levels of the tracheobronchial circulation (arteries, veins and bronchopulmonary anastomoses). These responses are mediated via muscarinic receptors. Vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (in man peptide histidine methionine) are the main mediators of the noncholinergic nerves. Both of them produce vasodilation in the tracheobronchial circulation; VIP can cause longer-lasting responses with larger doses. The afferent or sensory nerves contain tachykinins, i.e. substance P and neurokinins A and B, which are potent vasodilators in the tracheobronchial circulation and also potent inducers of postcapillary permeability. Calcitonin gene-related peptide is another sensory neuropeptide with ability to produce long-lasting vasodilations without affecting microvascular permeability.