Abstract
The effects of ACh and histamine on electrical and mechanical properties of intrapulmonary artery and vein muscles were studied in rats. In the artery, ACh and histamine indirectly relaxed the precontracted muscles in high-[K]o solution via the release of endothelium-derived relaxing factor (EDRF) from the endothelial cells, and also produced contractions by acting directly to the muscles. ACh and histamine elicited a transient hyperpolarization of the arterial smooth muscle membrane mainly due to an increase in K permeability, only in the presence of endothelial cells. In the absence of endothelial cells, histamine and ACh depolarized the arterial smooth muscles. The intrapulmonary vein consisted of the invaded cardiac muscles; and ACh, but not histamine, hyperpolarized the membrane of these muscles by an increase in K permeability, with no relationship to the endothelial cells. It is concluded that in the rat intrapulmonary artery, ACh and histamine elicit excitatory and inhibitory responses in hese vascular muscles in direct and indirect manners. The indirect actions involve relaxing and hyperpolarizing factors released from the arterial endothelial cells. ACh but not histamine elicited inhibitory responses to the intrapulmonary vein muscles in a direct manner.
