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K Sumimoto

Publications and source records attributed to K Sumimoto.

72 records · Page 4Linked to original sources
PubMed1987

Effects of procaine on pharmaco-mechanical coupling mechanisms activated by acetylcholine in smooth muscle cells of porcine coronary artery.

The action of procaine on pharmaco-mechanical coupling activated by application of acetylcholine (ACh) was investigated using collagenase-treated dispersed intact and skinned smooth muscle cells and intact muscle tissues of the porcine coronary artery. ACh reduced stored 45Ca2+, and this action was prevented by procaine in intact dispersed cells. The maximum reduction in the level of stored 45Ca induced by caffeine (25 mM) or inositol 1,4,5-trisphosphate (InsP3; 3 microM) was also prevented by procaine in the skinned muscle cells in the presence or absence of ATP. However, inhibitions of the latter required higher concentrations of procaine than the former. Release by 10 microM ACh of Ca2+ from its store site in the presence or absence of extracellular Ca2+ was also inhibited by procaine and was detected using the quin2 fluorescence method. In these smooth muscle tissues, ACh (above 10 nM) reduced the amount of phosphatidylinositol 4,5-bisphosphate (PI-P2) and dose dependently increased the amount of phosphatidic acid. Procaine inhibited the hydrolysis of PI-P2 activated by ACh, thus reducing the amount of InsP3 and the release of Ca2+ from the store site. It is concluded that procaine has multiple actions on the porcine coronary artery, and one of the actions related with pharmacomechanical coupling appears through inhibition of hydrolysis of PI-P2 induced by ACh.

Acetylcholine↗
PubMed1987

Actions of nicorandil on vascular smooth muscles.

The action of nicorandil on vascular smooth muscles has been studied in vitro using the microelectrode, Ca-transient, isometric tension recording methods, and the bioassay methods of cyclic nucleotides and inositol phospholipids. Nicorandil increased Ca-insensitive K conductance and hyperpolarized the membrane and thus prevented the activation of the voltage-dependent Ca channel. The hyperpolarization occurred to a greater extent in venous tissue than in arterial tissue. Nicorandil stimulated the synthesis of cyclic guanosine monophosphate (cGMP) in the polarized and depolarized muscle tissues, as did nitroglycerin. Consequently, nicorandil reduces the concentrations of free Ca in the myoplasm, due to acceleration of the Ca pump at the sarcolemma, and may prevent the phosphorylation of myosin through phosphorylation of myosin light chain kinase. These actions of nicorandil may not contribute to the synthesis of inositol-1,4,5-trisphosphate hydrolyzed from phosphatidylinositol-4,5-bisphosphate. The above actions of nicorandil--hyperpolarization and increase in the cyclic GMP--may cause relaxation of the tissues precontracted by various stimulants.

Action Potentials↗
PubMed1987

Ischemic damage prevention by coenzyme Q10 treatment of the donor before orthotopic liver transplantation: biochemical and histologic findings.

This study was undertaken to determine whether pretreatment of the donor rat with coenzyme Q10 (CoQ10) would protect against hepatic ischemia induced for 30 minutes at normothermic body temperature. Fresh liver transplants were used as controls (minus warm ischemia of 30 minutes) and gave a 1-week survival rate of 84.6%. CoQ10 was administered intravenously (10 mg/kg body weight) to the donor rat 1 hour before induction of warm ischemia (group A). In another group (B), the same dose was given intravenously not only to the donor rat but also to the recipient rat 1 hour before grafting. None of the placebo group survived more than 2 days. The 1-week survival rates of the groups pretreated with CoQ10 were 45.5% for group A and 50% for group B. There was no significant difference between groups A and B. A statistically significant difference was demonstrated between the placebo group and both CoQ10-treated groups (p less than 0.05). It was therefore assumed that CoQ10, accumulated in the donor liver, was a primary factor in improving survival. Serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), serum alkaline phosphatase (SALP), total bilirubin, and total protein were measured by means of light and electron microscopic examination of the liver 6 months after transplantation. Long-term-surviving rats with transplanted, ischemically damaged liver that was pretreated with CoQ10 showed a decrease in the activity of SGOT and SGPT and an increase in levels of total protein to the normal range (as well as to those levels exhibited by fresh-liver-transplanted rats) with practically no change in levels of SALP, total bilirubin, or in histologic findings. These results indicate that donor pretreatment with CoQ10 is useful for increasing survival after warm ischemic damage of rat liver grafts.

Alanine Transaminase↗
PubMed1986

Mobilization of free Ca2+ measured during contraction-relaxation cycles in smooth muscle cells of the porcine coronary artery using quin2.

Ca2+ mobilization in dispersed smooth muscle cells of the porcine coronary artery was investigated using the fluorescent Ca2+ indicator, quin2. The resting [Ca2+]i was 113 +/- 8 nM (a mean +/- SE), and was independent of intracellular quin2 concentrations. Acetylcholine (ACh; over 10 nM) or caffeine (over 3 mM) transiently increased the intensity of fluorescence, thereby reflecting the elevation of intracellular free Ca2+ (Ca2+ transient), while excess K+ gradually increased and maintained the intensity of fluorescence. Application of EGTA reduced the resting intensity of the fluorescence and blocked the K+-induced Ca2+ transient, but did not suppress the ACh- or caffeine-induced ones. Nisoldipine (0.1 microM) did not affect the resting intensity of the fluorescence. This agent blocked the K+ induced but not the ACh- or caffeine- induced Ca2+ transient. Thus, sources of Ca2+ contributing to the K+ -induced Ca2+ transient differ from those evoked by other agents. The amount of Ca2+, as estimated from the increased Ca2+ transient by caffeine or ACh, was increased in proportion to the excess K+-induced influx of Ca2+.

Acetylcholine↗
PubMed1986

A phorbol ester has dual actions on the mechanical response in the rabbit mesenteric and porcine coronary arteries.

To clarify the role of protein kinase C in the mechanical response, the effects of 12-o-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, were investigated on intact and skinned smooth muscle preparations of the rabbit mesenteric artery. TPA (0.1 microM) showed dual actions (initial enhancement followed by inhibition during long exposure) on the K+-induced contraction. The enhancement was marked in the presence of 39 mM-K+ but inhibition was the predominant effect in the presence of 128 mM-K+. Addition of 2.6 mM-Ca2+ to a Ca2+-free solution containing 2 mM-EGTA following application of A23187 (1 microM), produced contraction. TPA showed the same dual actions on this Ca2+-induced contraction. In chemically skinned muscles, TPA increased the amplitude of Ca2+-induced contractions evoked by low concentrations of Ca2+ (0.1-0.3 microM), but reduced those evoked by high concentrations of Ca2+ (1-10 microM). Both actions of TPA were facilitated in the presence of phosphatidylserine (PS). TPA with PS had no effect on the Ca2+-independent contraction evoked in relaxing solution containing 10 mM-EGTA and 4 mM-Mg ATP following application of adenosine-5-o-3-thiotriphosphate (ATP gamma S) and 0.3 microM-Ca2+. The amount of Ca2+ stored in cells estimated from the amplitude of the caffeine-induced contraction was not modified by application of TPA with PS in skinned or intact muscle tissues. The effects of TPA were investigated on the Ca2+ transient measured from the intensity of fluorescence of quin-2 in dispersed cell suspensions prepared from the porcine coronary artery. TPA had no effect on the Ca2+ transient in high K+ but enhanced the amplitude of the contraction. Amplitudes of the tonic response evoked by 39 mM-K+ in intact muscle tissues and the contraction induced by 0.3 microM-Ca2+ in skinned muscle were much the same. TPA with PS enhanced the amplitudes of both contractions to the same extent. From the above results, we concluded that TPA shows dual actions on the contractile machinery and may act on the regulatory systems of contractile proteins. Both excitatory and inhibitory actions of TPA depended on the concentration of Ca2+. However, the physiological action of protein kinase C as estimated from the action of TPA seems to be related to an excitatory action on the contractile machinery.

Animals↗
PubMed1985

[Results of registration of gynecologic malignant neoplasms in Shizuoka Prefecture--evaluation for one and a half years].

To eliminate death by cancer, it would be necessary for us to register newly developed cancer in certain districts. We have registered all gynecologic malignant neoplasms in Shizuoka Prefecture, Japan, since October 1982 using a microcomputer. Analysis for one and a half years was performed as follows. Gynecologic malignancies are as detailed below: cervical cancer 304 cases, corpus cancer 58 cases, ovarian cancer 51 cases, vaginal cancer 4 cases, vulvar cancer 5 cases. A study of the correlation between detected malignancies and gynecologic examinations, particularly concerning cytologic check-up, revealed the importance of cytology in early cancer detection.

Adult↗
PubMed1984

Neurological control of fetal heart rate in 20 cases of anencephalic fetuses.

Fetal heart rate (FHR) is influenced by the central nervous system, cardiac automatism, biochemical factors, etc. Changes in FHR were correlated with the anatomic defect in autopsy material from 20 anencephalic infants, and, on this basis, the following hypotheses were formed, subject to later experimental proof. (1) The FHR baseline level is controlled by the medulla oblongata and vagus nerve. (2) The biphasic sleep-awake pattern is controlled by the cerebral cortex. (3) The midbrain is involved in the occurrence of acceleration. (4) A relative high level of short-term variability is shown when small lesions of the lesser central nervous system are present, but we cannot conclude that the cortex is critical for short-term variability. On the other hand, long-term variability seems to be correlated to the presence of the medulla oblongata and midbrain, and might be amplified by the cerebral cortex. (5) U-shaped decelerations are connected with the medulla oblongata, but V-shaped decelerations depend on intracardiac reflexes and myocardial stretch.

Anencephaly↗