FIGURE 6.

Schematic diagram summarizing autonomic neural mechanisms controlling pulmonary vascular tone. Afferent neural signals arise from pulmonary baroreceptors, systemic arterial baroreceptors and metabolically responsive skeletal muscle afferents (metaboreceptors). These have stimulatory effects (vasoconstricting; black arrows) and inhibitory effects (vasodilatory; red T‐shaped lines) on pulmonary vascular tone and stiffness. These afferent inputs are likely to be integrated in the CNS with efferent parasympathetic and sympathetic responses exerted through vagal and sympathetic efferents to the pulmonary vasculature, respectively. Sympathetic efferents increase vascular tone and stiffness via α‐adrenergic signalling (α) and reduce vascular tone and stiffness via β‐adrenergic signalling (β). ATP and neuropeptides, such as neuropeptide Y (NPY), might also be vasoconstrictive sympathetic neurotransmitters. Parasympathetic activation, predominately via cholinergic transmission (ACh), exerts dual effects of vasodilatation and reduced stiffness, mediated via the endothelium (Endo) and nitric oxide (NO), and vasoconstriction and increased stiffness, mediated via the action of vascular smooth muscle (VSMC). Vasoactive intestinal peptide (VIP) and NO also act as vasodilatory neurotransmitters for parasympathetic neurons. Created in BioRender. Plunkett, M. (2024) BioRender.com/e97z759.