ISSN: 1755-5310 (Electronic)1755-5302 (Print)

Interventional Cardiology

Journals On Pulmonary Circulation

The pulmonary circulation is supplied with both sympathetic and parasympathetic innervation. In general, increased sympathetic activity leads to release of catecholamines (e.g., dopamine, norepinephrine, epinephrine, and neuropeptide Y) that cause vasoconstriction and an increase in pulmonary vascular resistance. Pulmonary arteries contain fewer cholinergic than adrenergic nerve fibers. Parasympathetic stimulation causes the release of acetylcholine and vasoactive intestinal polypeptide, which mediate vascular dilation and a decrease in pulmonary vascular resistance. The lung also contains nonadrenergic, noncholinergic nerves that can be excitatory (e-NANC) or inhibitory (i-NANC). Release of vasoactive intestinal peptide, calcitonin gene-related peptide, substance P, and nitric oxide from i-NANC nerves mediates vasodilation, while the e-NANC nerves mediate vasoconstriction, although the neurotransmitter involved remains unclear. Curiously, in contrast to the systemic vasculature, there appears to be minimal nervous control in the pulmonary circulation with respect to basal vascular caliber. Moreover, while the existence and activity of e-NANC and i-NANC nerves have been demonstrated in vitro, regulation of tone in vivo by these nerves has not been demonstrated. However, stimulation of adrenergic nerves may modulate pulmonary vascular resistance and blood flow during exercise and cold exposure and may increase in regulatory contribution during pathological states, particularly during pulmonary edema and embolism.    

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