Publications by authors named "Sunano S"

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.

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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.

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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.

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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.

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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.

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1. There are known differences in the sensitivity to caffeine between skeletal muscle (soleus) of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The present study was performed in order to examine differences in the effects of caffeine on twitch contraction between visceral striated muscle using the outer layer of the oesophagus from WKY rats and stroke-prone SHR (SHRSP).

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To elucidate whether properties of the sarcoplasmic reticulum are altered, not only in vascular smooth muscle, but also in visceral striated muscle of spontaneously hypertensive rats (SHR), caffeine-induced contractures in oesophageal striated muscle of Wistar Kyoto rats (WKY) and stroke-prone SHR (SHRSP) were compared. In both preparations, 30 mM caffeine induced a contracture with two components. The second component, which was diminished by extracellular Ca(2+) removal or Ni(2+) but not by verapamil, was much smaller in SHRSP.

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To evaluate whether the elevated blood pressure induced by chronic treatment with N(omega)-nitro-L-arginine methyl ester (L-NAME) contributes to an impairment of endothelium-dependent relaxation (EDR), the effects of chronic treatment of Wistar rats with L-NAME on systolic blood pressure, pulmonary arterial blood pressure and EDR of the pulmonary arteries were studied and compared with those of stroke-prone spontaneously hypertensive rats (SHRSP). While the systolic blood pressure (SBP) of Wistar rats was increased above that of controls by chronic treatment with L-NAME, it was still significantly lower than that of SHRSP. Chronic treatment with L-NAME did not affect pulmonary arterial blood pressure.

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1. Responses to endothelium-derived nitric oxide (EDNO), indomethacin-sensitive endothelium-derived contracting factor (EDCF) and hyperpolarization by endothelium-derived hyperpolarizing factor (EDHF) and the interaction among these factors in mesenteric arteries from 16-week-old Wistar Kyoto (WKY) rats and age-matched stroke-prone spontaneously hypertensive rats (SHRSP) were studied, observing the time-course of the response to 10-5 mol/L acetylcholine (ACh). 2.

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Endothelium-removed carotid artery strips from stroke-prone spontaneously hypertensive rats spontaneously developed a tonic myogenic contraction. Flufenamic acid reduced the resting tone observed during superfusion with Tyrode's solution, in a concentration-dependent manner. Flufenamic acid also inhibited contractions produced by high-K solutions in a concentration-dependent manner.

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Caffeine-induced relaxation was studied in aortic segments from Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Although acetylcholine-induced endothelium-dependent relaxation was impaired in preparations from SHRSP, the relaxation induced by caffeine was identical in both groups. In addition, caffeine-induced relaxation was not affected by removal of the endothelium in either group.

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C-kit immunoreactive cells are known to be interstitial cells of Cajal (ICCs), and they generate pacemaker activity of the gastrointestinal tract. Recently a large number of special smooth muscle cells corresponding to c-kit immunoreactive cells were found in the proximal colon of the guinea pig. We learned that the rat proximal colon showed tetrodotoxin-insensitive regular rhythmic spontaneous contractions (RSCs) and hypothesized that RSCs are generated and/or regulated by ICCs.

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The effects of NG-nitro-L-arginine (L-NNA) on blood pressure of various strains of spontaneously hypertensive rats were studied. Blood pressure of the rats was higher in the order of WKY, SHR, SHRSP, M-SHRSP. L-NNA caused an elevation of the blood pressure, which was greatest in SHR and smallest in WKY and M-SHRSP.

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Effects of chronic treatment of normotensive Wistar rats with N(omega)-nitro-L-arginine methyl ester (L-NAME) on blood pressure and on endothelium-dependent relaxation of the aorta, carotid and iliac arteries were studied. The endothelium-dependent relaxation was compared in arteries from normotensive Wistar Kyoto rats (WKY) and genetically hypertensive rats (stroke-prone spontaneously hypertensive rats, SHRSP). Chronic treatment of normotensive Wistar rats with L-NAME caused an elevation of blood pressure.

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The time course of the response to prolonged application of acetylcholine in mesenteric arteries from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY) was compared. Only a relaxing response, which was blocked by N(omega)-nitro-L-arginine (L-NOARG), was observed after the prolonged application of a low concentration of acetylcholine (10(-8) M) in both preparations; the response was impaired in SHRSP preparations. Prolonged application of a high concentration of acetylcholine (10(-5) M) induced a second contractile response after a first relaxing response in SHRSP preparations under basal conditions and in WKY preparations in the presence of L-NOARG.

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Difference in effects of stretch tension on endothelium-derived nitric oxide (EDNO)-dependent depression of noradrenaline (NA)- and high-K+-induced contraction between the aortae from normotensive Wistar Kyoto rats (WKY) a nd stroke-pronespontaneously hypertensive rats (SHRSP) was studied. NA-induced contraction in preparations both from WKY and SHRSP was augmented in the presence of N(omega)-nitro-L-arginine (L-NNA). This augmentation was minimized when the spontaneous tone, which was more prominent in preparations from SHRSP, was subtracted and the effects of L-NNA became less prominent in preparations from SHRSP.

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Hepatic arteries are reportedly innervated by vasoconstrictor and vasodilator nerves. Experiments were carried out to investigate the possible involvement of calcitonin gene related peptide (CGRP) and nitric oxide as neurotransmitters during the relaxation of the rat common hepatic artery produced by transmural electrical field stimulation (ES). Common hepatic arteries were excised under ether-anesthesia from 6 weeks-old female rats, and isometric tensions recorded from endothelium-damaged ring preparations.

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The role of nitric oxide in the electrical and mechanical activities of the rat portal vein was examined in circular muscle preparations with intact endothelium that were isolated from the longitudinal muscle layer. In contrast to the longitudinal muscle preparation, the circular muscle preparation did not show spontaneous phasic contraction. Inhibition of nitric oxide synthesis by Nomega-nitro-L-arginine (L-NNA) induced a tonic contraction.

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Endothelium-dependent relaxation of aorta and carotid artery from stroke-prone spontaneously hypertensive rats (SHRSP) and the effect of chronic treatment of SHRSP with perindopril, an angiotensin converting enzyme inhibitor, on endothelium-dependent relaxation were studied. Endothelium-dependent relaxation was induced by acetylcholine (ACh) in preparations of SHRSP and normotensive Wistar Kyoto rats (WKY) precontracted with noradrenaline. The ACh-induced relaxation in both preparations was abolished by L-nitroarginine.

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Effects of isoproterenol on contraction and membrane potential of gastric smooth muscle were studied in stroke prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY). Circular muscle preparation from the gastric fundus developed tonic contraction by re administration of Ca2+ to a nominally Ca2+-free solution. The contraction was inhibited by nifedipine or nicardipine.

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Involvement of endothelium-derived nitric oxide (EDNO) in alpha-adrenoceptor agonist-induced contractile responses was studied in isolated pulmonary arteries from Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). In the presence of propranolol, noradrenaline-induced contraction was potentiated by endothelium removal or by N(G)-nitro-L-arginine (L-NOARG). The magnitude of the potentiation was independent of the noradrenaline concentration.

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1. The effects of cyclopiazonic acid (CPA), a selective inhibitor of sarcoplasmic reticulum (SR) Ca2+-ATPase, on twitch contraction and on the resting state of tension and intracellular Ca2+ level ([Ca2+]i) of the oesophageal striated muscle of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY) were compared. 2.

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Control of the active tone by endothelium in aortae from various strains of spontaneously hypertensive rats was studied. The active tone was negligibly observed in endothelium-intact preparation. The application of N(G)-nitro-L-arginine (L-NNA, 10(-4) M) induced slowly developed active tone in the preparations from hypertensive rats but no active tone was induced in the preparation from normotensive Wistar Kyoto rats (WKY).

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Influences of endothelium on contraction of aortic smooth muscle by various agents were studied and those in the preparations from Wistar Kyoto rat (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were compared. Endothelium depressed the contractions induced by noradrenaline and 5-hydroxytryptamine (5-HT). The time course of the contraction was bi- or tri-phasic in the former and slow rising monophasic in the latter.

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1. The mechanisms of oscillatory contraction of arterial smooth muscle in vitro are discussed. 2.

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