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Am J Physiol Heart Circ Physiol 279: H1786-H1795, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H1786-H1795, October 2000

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

Kaoru M. Ito1, Miharu Sato1, Keiko Ushijima1, Masaaki Nakai2, and Katsuaki Ito1

Departments of 1 Veterinary Pharmacology and 2 Anatomy, Faculty of Agriculture, Miyazaki University, Miyazaki 889-2192, Japan

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 -48.3 ± 2.6 and -39.8 ± 2.2 mV at 2 and 3 wk after treatment with MCT, respectively (control arteries -59.9 ± 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. Nomega -nitro-L-arginine (200 µM), 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.

nitric oxide; membrane potential; depolarization; sodium nitroprusside; resting tone


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