AUTHOR=Lo Charmaine C. W. , Moosavi Seyed M. , Bubb Kristen J. TITLE=The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension JOURNAL=Frontiers in Physiology VOLUME=9 YEAR=2018 URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2018.01167 DOI=10.3389/fphys.2018.01167 ISSN=1664-042X ABSTRACT=
Pulmonary hypertension (PH) is an incurable, chronic disease of small pulmonary vessels. Progressive remodeling of the pulmonary vasculature results in increased pulmonary vascular resistance (PVR). This causes secondary right heart failure. PVR is tightly regulated by a range of pulmonary vasodilators and constrictors. Endothelium-derived substances form the basis of most current PH treatments. This is particularly the case for pulmonary arterial hypertension. The major limitation of current treatments is their inability to reverse morphological changes. Thus, there is an unmet need for novel therapies to reduce the morbidity and mortality in PH. Microvessels in the lungs are highly innervated by sensory C fibers. Substance P and calcitonin gene-related peptide (CGRP) are released from C-fiber nerve endings. These neuropeptides can directly regulate vascular tone. Substance P tends to act as a vasoconstrictor in the pulmonary circulation and it increases in the lungs during experimental PH. The receptor for substance P, neurokinin 1 (NK1R), mediates increased pulmonary pressure. Deactivation of NK1R with antagonists, or depletion of substance P prevents PH development. CGRP is a potent pulmonary vasodilator. CGRP receptor antagonists cause elevated pulmonary pressure. Thus, the balance of these peptides is crucial within the pulmonary circulation (