Neural control of airway vasculature and edema

Abstract

The tracheobronchial vasculature is controlled by adrenergic, cholinergic, and peptidergic nervous mechanisms. Sympathetic nerves release norepinephrine and neuropeptide Y (NPY), which are both constrictor agents, the latter being long-lasting. Parasympathetic nerves release acetylcholine and usually vasoactive intestinal polypeptide (VIP), both of which are vasodilators, VIP being the longer lasting. These motor nerves are controlled by many reflex inputs. Activation of pulmonary C-fiber receptors by irritants and inflammatory mediators causes a powerful vasodilatation, mainly via sympathetic motor nerves. Cardiac and chemoreceptor reflexes also influence airway vascular tone. Sensory nerves in the airway mucosa are responsible for local axon reflexes in response to irritants and inflammatory mediators. These nerves contain neuropeptides such as substance P (SP), neurokinins A and B (NKA, NKB), and calcitonin gene-related peptide (CGRP). All these neuropeptides are powerful vasodilators. Thus, inflammatory conditions in the lungs such as asthma cause vasodilation by local direct action of mediators, by axon reflexes, and by central nervous reflexes. The vasodilation could lead to mucosal edema. Thus, airway vascular responses have to be added to bronchoconstriction and mucus secretion as part of the mucosal pathology of asthma.