Abstract

Based upon catecholamine histofluorescence and capacity for neuronal uptake of norepinephrine, extra- and intrapulmonary arteries are well supplied by adrenergic nerves. In isolated segments of arteries larger than 0.6 mm in diameter, these nerves release sufficient transmitter to cause vasoconstriction. However, in arteries smaller than 0.6 mm in diameter, both nerve stimulation and NE application elicited either very small responses or none at all. The vascular smooth muscle was responsive under the experimental conditions, since all arterial segments constricted in response to 5HT, histamine, and KCl, and the maximal effects of the three agents were equal. It is not yet known whether the poor reactivity of small arteries to NE and adrenergic nerve stimulation is peculiar to the rabbit pulmonary vascular bed, and whether segments of the pulmonary vascular tree farther downstream than those studied are more reactive to sympathetic stimulation. Possibly the sympathetic control of vascular tone is restricted to the relatively large arteries. Reduction in the magnitude of the contractile response, rather than sensitivity to NE, appears to account for the diminution of vessel response as the vessel becomes smaller. It is speculated that, in the pulmonary vasculature through which the output of the right heart passes to the left, an extensive arterial constriction accompanying sympathetic discharge resulting in major changes in blood flow is undesirable.

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