Neural and Humoral Factors Cause Contraction of the Muscular Pulmonary Arteries
A variety of neural and humoral factors can contract or relax pulmonary vascular smooth muscle and thereby alter the resistance to blood flow. The magnitude of the response of vessels to these stimuli is largely determined by the amount of smooth muscle in the small pulmonary arteries, which varies with species (Figure 46-6).
The increase in pulmonary vascular pressure in response to alveolar hypoxia and other stimuli is greater in calves than in sheep because of the greater amount of smooth muscle in Calfpulmonaryarteries.AlthtJUgh pulmonary arteries have both sympathetic and parasympathetic innervation, the functional role of this autonomic innervation is unclear. Ttble 46-1 lists the responses of the pulmonary vasculature to a variety of chemical mediators. Responses may vary among species and with the initial degree of vascular tone. Some mediators, such as acetylcholine and bradykinin, relax smooth muscle and cause vasodilation by
Pulmonary Vascular Response to Chemical Mediators
| Agent | Action |
| Angiotensin Il Histamine (H1, H2) | Vasoconstriction Usually vasoconstriction through H1 receptors; if vascular tone elevated, vasodilation through H2 receptors; acts on both arteries and veins |
| Scrotonin (5 HT2) Norepinephrine, phenylephrine | Vasoconstriction though 5-HT2 receptors; action restricted to pulmonary arteries Vasoconstriction through α1- and α2-adrenergic receptors |
| Epinephrine | Vasoconstriction or vasodilation, depending on resting vascular tone and predominance of α or β-adrenergic receptors. |
| Isoproterenol | Vasodilation through β receptors |
| Acetylcholine | Vasodilation through release of nitric oxide when endothelium intact. Vasoconstriction when endothelium removed. |
| Bradykinin | Variable; usually vasodilation; acts through release of vasoactive prostaglandins and nitric oxide |
| Arachidonic acid Prostacyclin* | Usually vasoconstriction Vasodilation |
| Thromboxane Leukotrienes | Vasoconstriction Usually vasoconstriction |
•Prostaglandin I2(PGI2).
releasing nitric oxide (NO) or vasodilator prostaglandins from the endothelium. Release of NO also occurs in response to the increased shear stress across the endothelium when blood flow increases. The increased NO release may be partly responsible for the dilation of the pulmonary circulation during exercise. Catecholamines, bradykinin, and prostaglandins are metabolized by the vascular endothelium, so their effects may be modified by endothelial damage.