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Sympathetic nerve fibers of the main pulmonary arteries are components of the autonomic nervous system that innervate the large pulmonary arteries. They arise from the thoracic sympathetic trunk, travel through the pulmonary plexus, and predominantly release noradrenaline (norepinephrine), which acts primarily on α₁-adrenoreceptors on vascular smooth muscle to increase pulmonary vascular resistance and decrease compliance[1][3][5][8]. In humans and larger mammals, these fibers extend throughout the main and larger intrapulmonary arteries, but not into the smallest arterioles[1]. Their physiological function includes the reflexive adaptation of the pulmonary vasculature to changes in arterial pressure and hypoxia (e.g., during increased pulmonary blood flow or systemic stress)[1][5]. They colocalize with neuropeptides such as neuropeptide Y (NPY) and sometimes dynorphin[1]. While disruption or modulation of these fibers can alter pulmonary hemodynamics—and has been studied as a contributor to diseases like pulmonary hypertension—they are not a discrete molecular target (such as a receptor, channel, or enzyme) but rather a component of neurovascular anatomy. Thus, the entry is not a valid molecular therapeutic target in the standard sense, although autonomic modulation (e.g., by neuroablation techniques) can have disease-modifying effects[3][5].
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