Alterations of endothelium and smooth muscle function in monocrotaline-induced pulmonary hypertensive arteries

Kaoru M. Ito, Miharu Sato, Keiko Ushijima, Masaaki Nakai, Katsuaki Ito
2000 American Journal of Physiology. Heart and Circulatory Physiology  
Alterations of endothelium and smooth muscle function in monocrotaline-induced pulmonary hypertensive arteries. Am J Physiol Heart Circ Physiol 279: H1786-H1795, 2000.-We examined how monocrotaline (MCT), which impairs the endothelium and causes pulmonary hypertension, altered the endothelial regulation of pulmonary artery functions. Rats were given a single injection of MCT (60 mg/kg sc). Pulmonary arteries were depolarized to Ϫ48.3 Ϯ 2.6 and Ϫ39.8 Ϯ 2.2 mV at 2 and 3 wk after treatment with
more » ... er treatment with MCT, respectively (control arteries Ϫ59.9 Ϯ 1.9 mV). The basal tone in the resting state was only slightly elevated at 3 wk in endothelium-intact arteries. Removal of the endothelium caused further depolarization in MCT-affected arteries at 2 wk, but not at 3 wk, and greatly elevated the basal tone at 2 and 3 wk. N -nitro-L-arginine (200 M), a nitric oxide synthase inhibitor, also caused depolarization in endothelium-intact arteries in both groups and elevated the basal tone of MCT-affected arteries. The relaxant responses of pulmonary arteries to ACh and A-23187 were depressed at 2 and 3 wk after MCT treatment. Thus chronic impairment of the endothelium altered the property of the pulmonary artery leading to depolarization. During the early stage of depolarization, a rise in the basal tone was offset by nitric oxide released from the injured endothelium.
doi:10.1152/ajpheart.2000.279.4.h1786 pmid:11009465 fatcat:r7nhfuutrvhirfn5ojysxbafka