Superoxide dismutase reduces the impairment of endothelium-dependent relaxation in the spontaneously hypertensive rat aorta.

The involvement of the superoxide anion in endothelium-dependent relaxation (EDR) was examined in noradrenaline-contracted aortic smooth muscle preparations isolated from normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Acetylcholine (ACh, 10(-9)-10(-5) M) induced EDR in both WKY and SHRSP preparations in a concentration-dependent manner, but with a significantly smaller amplitude in those from SHRSP than in those from WKY. The ACh-induced EDR was inhibited by N(omega)-nitro-L-arginine (L-NOARG), in a concentration-dependent manner, both in WKY and SHRSP.

Abnormal response to ryanodine in oesophageal striated muscle of spontaneously hypertensive rats.

The effects of ryanodine on twitch contraction and basal tension of oesophageal striated muscle were compared between preparations from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY). Ryanodine (3 x 10(-7) M) augmented the twitch contraction in WKY preparations, butt attenuated it in SHRSP preparations. Rates of contraction and relaxation of twitch contraction, normalized to developed tension, were slightly decreased by ryanodine in both preparations.

[Endothelium-derived factors in hypertensive blood vessels, especially nitric oxide and hypertension].

Endothelium-dependent relaxation (EDR) in the blood vessels of spontaneously hypertensive rats (SHR) and the role of nitric oxide (NO) in the initiation of hypertension are reviewed. EDR was impaired in blood vessels of SHR depending on age and degree of hypertension when compared with those of normotensive rats. The cause of the impairment varied among the type of blood vessels: a decrease in the production of NO and endothelium-derived relaxing factor (EDRF) and an increase in the production of endothelium-derived contracting factor (EDCF) are the main causes of the impairment in large arteries, while a decrease in endothelium-dependent hyperpolarization and increased release of EDCF are the main causes of the impairment in small arteries.

Contraction of arterial smooth muscle of normotensive and spontaneously hypertensive rats by manganese(III)tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP).

Manganese(III)tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP), which has been known as a cell permeable superoxide dismutase mimetic, induced concentration-dependent contraction in rat carotid artery acting directly on smooth muscle. The contractile action was more prominent in the preparation from stroke-prone spontaneously hypertensive rats (SHRSP) compared with that from Wistar Kyoto rats (WKY). It was abolished by the removal of extracellular Ca(2+) or the application of verapamil.

Effects of L-arginine on spontaneous contraction of the rat portal vein.

The effects of L-arginine on spontaneous contraction of endothelium-denuded longitudinal preparations of the rat portal vein were studied. L-arginine increased the frequency of spontaneous contraction concentration-dependently between 10 microM and 1 mM. Changes in contraction amplitude and duration were not remarkable.