PubMed Health⌕ Search

Biomedical subjects

H Ohshika

Publications and source records attributed to H Ohshika.

At least 37 records · Page 2Linked to original sources

Relation between spontaneous contraction and sarcoplasmic reticulum function in cultured neonatal rat cardiac myocytes.

The relation between spontaneous contraction, Ca2+ oscillations, and sarcoplasmic reticulum (SR) function was studied in cultured neonatal rat cardiac myocytes. Spontaneous contraction and Ca2+ oscillations were irregular at day 2 of culture but became regular at day 6 of culture in neonatal rat cardiac myocytes. The rate of spontaneous contraction and the frequency of Ca2+ oscillations were decreased by verapamil and were abolished in the absence of extracellular Ca2+ at both day 2 and day 6 of culture. Ryanodine and thapsigargin increased the rate of contraction and the frequency of Ca2+ oscillations at day 2 of culture but did not affect contractions and Ca2+ oscillations at day 6 of culture. Ultrastructural observation showed that the structure of SR developed less at day 6 of culture. The present results suggest that spontaneous contraction and Ca2+ oscillations are due mainly to extracellular Ca2+ influx but not to Ca2+ release from SR in neonatal rat cardiac myocytes.

Animals↗

Comparative myocardial depression of sevoflurane, isoflurane, and halothane in cultured neonatal rat ventricular myocytes.

UNLABELLED: In this study, we compared the direct myocardial depressant effects of sevoflurane, isoflurane, and halothane and determined whether an L-type Ca2+ channel agonist, Bay K 8644, could attenuate the myocardial depression induced by these anesthetics in cultured neonatal rat ventricular myocytes. Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 6-7 days. The myocytes were stabilized in serum-free medium, and the spontaneous beating rate and contractile amplitude were measured by using a fiberoptic sensor. Each anesthetic decreased the beating rate and amplitude in a concentration-dependent manner (1%-4% vol/vol) (P < 0.001), with halothane decreasing the beating rate and amplitude the most (P < 0.01). Isoflurane caused larger decreases in the beating rate than sevoflurane at 3% and 4% (P < 0.05). Potency for suppression of contractile amplitude was in the order of halothane > > isoflurane > sevoflurane. However, the myocardial depressant effects of the anesthetics were not different when their concentrations were corrected for minimum alveolar anesthetic concentration values. Bay K 8644 significantly prevented the anesthetic-depressed amplitude (P < 0.05). We conclude that sevoflurane, isoflurane, and halothane have direct myocardial depressant effects on cultured neonatal rat ventricular myocytes and that the reduction of sarcolemmal L-type Ca2+ channel current levels mediates the myocardial depression observed in these immature hearts. IMPLICATIONS: Sevoflurane, isoflurane, and halothane have a direct cardiodepressant effect on cardiac excitation-contraction coupling in the immature heart, which is mediated by an interaction with the L-type Ca2+ channel.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Mechanism of endothelin-1 release from endothelial cells in pregnancy-induced hypertension.

We investigated the mechanism of vasoconstrictor-induced endothelin-1 (ET-1) release from human umbilical vein endothelial cells (HUVECs) in serum from women with pregnancy-induced hypertension (PIH). We obtained serum samples from seven women with PIH, seven healthy nonpregnant women (NP), and seven normal pregnant women (NPIH). ET-1 and inositol 1,4,5-trisphosphate (IP3) were assayed by ET-1 ELISA and an IP3 3H assay system, respectively. ET-1 release from HUVECs incubated with 10% serum (NP, NPIH, and PIH) was greater than that without human serum. Angiotensin II (Ang II)- and epinephrine (Epi)-induced ET-1 release were significantly increased by PIH serum. IP3 production in HUVECs incubated with 10% serum (NP, NPIH, and PIH) was greater than that without human serum. Ang II- or Epi-induced IP3 production in HUVECs incubated with PIH serum was increased but not significantly compared to that with other sera. Our results suggest that increased ET-1 release from HUVECs incubated with human serum may be mediated by IP3 production, but that Ang II- or Epi-induced ET-1 release from HUVECs incubated with PIH serum may be mediated by another mechanism.

Endothelin-1↗

Ruthenium red inhibits cytosolic Ca2+ oscillations induced by vasopressin in primary cultured hepatocytes.

The effects of ruthenium red were investigated on the vasopressin (Vp)-induced Ca2+ response in single, primary cultured rat hepatocytes loaded with fura-2. Low concentrations of Vp (1 nM) evoked a sustained train of baseline spike Ca2+ oscillations, with a latency to first peak of 170 s and a frequency of 0.37 min(-1). Treatment of hepatocytes with a higher concentration of Vp (10 nM) resulted in a rapid rise in intracellular Ca2+, with less delay (40 s), and which remained elevated and sustained. Microinjection of a low concentration of ruthenium red (10 microM in the injection pipette) altered the observed response to 1 nM Vp such that only 2 - 4 base line spikes were observed. A higher concentration of ruthenium red (50 microM in the injection pipette) completely abolished the 1 nM Vp response. However, the Ca2+ responses to higher concentrations of Vp (10 nM) or to the Ca2+-ATPase inhibitor, thapsigargin, were unaffected by ruthenium red. These results show that low concentrations of ruthenium red inhibit the Vp-induced oscillatory Ca2+ response and suggest a contribution of a ryanodine receptor-mediated Ca2+-induced Ca2+ release in generating the baseline spike oscillations in rat hepatocytes.

Animals↗

Effects of ondansetron on electrically evoked contraction in rat stomach fundus: possible involvement of 5-HT2B receptors.

This study examined the effects of ondansetron, an antagonist of the 5-hydroxytryptamine (5-HT3) receptor without 5-HT4 receptor agonistic activity. on electrically evoked contractions and acetylcholine release in rat stomach fundus strips. Ondansetron (10(-8)-10(-4) M) produced a concentration-dependent increase in the magnitude of the electrically evoked contraction, while it inhibited the release of acetylcholine induced by electrical field stimulation. The stimulatory effect of ondansetron (10(-6) M) on electrically evoked contractions was antagonized by yohimbine, a 5-HT2B receptor antagonist, but not by SDZ 205-557 (2-methoxy-4-amino-5-chloro-benzoic acid 2-[diethylamino] ethyl ester), a 5-HT4 receptor antagonist. In the presence of tetrodotoxin, ondansetron (10(-7)-10(-5) M) enhanced the contractions induced by acetylcholine. This stimulatory effect of ondansetron on acetylcholine-induced contractions was antagonized by yohimbine. These data suggest that ondansetron potentiates the contractile response to acetylcholine in the rat stomach fundus through the activation of 5-HT2B receptors.

Acetylcholine↗

Upregulation of expression of sarcoplasmic reticulum by TGF-beta 1 in cultured rat cardiac myocytes.

The effects of transforming growth factor-beta 1 (TGF-beta 1) on the function and structure of sarcoplasmic reticulum (SR) were studied in cultured neonatal rat cardiac myocytes. The cardiac myocytes at days 2 and 6 of culture exhibited spontaneous contraction; however, the rate of contraction increased and became regular, depending on culture day. Ryanodine and norepinephrine (NE) increased the rate of contraction and frequency of Ca2+ oscillations in myocytes at day 2 of culture. Ryanodine did not affect the spontaneous contraction in nontreated and TGF-beta 1-treated myocytes. On the other hand, NE caused negative and positive chronotropic responses in nontreated and TGF-beta 1-treated cells, respectively. In the absence of extracellular Ca2+, ryanodine and NE did not affect the cytoplasmic Ca2+ concentration ([Ca2+]i) in the nontreated cells, whereas NE increased [Ca2+]i but ryanodine did not in the TGF-beta 1-treated cells. SR structures in TGF-beta 1-treated cells developed more than those in nontreated cells. The results indicate that TGF-beta 1 plays an important role in the upregulation of SR function and structure of cultured neonatal rat cardiac myocytes.

Animals↗

Inhibitory effects of tetrandrine and hernandezine on Ca2+ mobilization in rat glioma C6 cells.

The effects of tetrandrine (TET), a Ca2+ antagonist of Chinese herbal origin, and hernandezine (HER), a structural analogue of TET, on Ca2+ mobilization were studied in rat glioma C6 cells. TET and HER alone did not affect the resting cytoplasmic Ca2+ concentration ([Ca2+]i). TET and HER inhibited the peak and sustained elevation of [Ca2+]i induced by bombesin and thapsigargin (TG), a microsomal Ca2+ ATPase inhibitor, in a dose-dependent manner. The doses of TET or HER needed to abolish the sustained and peak increase in [Ca2+]i induced by bombesin and TG were 30 microM and 300 microM, respectively. TET and HER did not increase inositol 1,4,5-trisphosphate (IP3) accumulation by themselves but inhibited IP3 accumulation elevated by bombesin. In permeabilized C6 cells, the addition of IP3 and TG released Ca2+ from intracellular stores. Pretreatment with TET or HER abolished Ca2+ release from intracellular stores induced by bombesin and TG. In the absence of extracellular Ca2+, the addition of 3 mM Ca2+ to extracellular medium slightly increased [Ca2+]i, which indicated Ca2+ entry due to leakage of Ca2+ at the plasma membrane but not Ca2+ influx through Ca2+ channels. TET and HER did not affect this leakage entry of Ca2+. The present results suggest that TET and HER inhibit Ca2+ release from intracellular stores as well as Ca2+ entry from extracellular medium evoked by bombesin and TG. In addition, TET and HER inhibit IP3 accumulation induced by bombesin in rat glioma C6 cells.

Alkaloids↗

Bilobalide, a constituent of Ginkgo biloba L., potentiates drug-metabolizing enzyme activities in mice: possible mechanism for anticonvulsant activity against 4-O-methylpyridoxine-induced convulsions.

Anticonvulsant effects of bilobalide, one of the constituents of Ginkgo biloba L., on the convulsions induced by 4-O-methylpyridoxine (MPN) were investigated in mice. Bilobalide reduced the duration and incidence of MPN-induced convulsions depending on its dose and the period of treatment. In addition, the anticonvulsant effect was manifested more than 24 hours after treatment and the effect lasted for 7 days after its withdrawal. In mice treated with bilobalide (30 mg/kg, p.o., once a day for 4 days), hepatic 7-methoxycoumarin O-demethylase activity was potentiated, and the disappearance of MPN in blood after MPN injection was faster than in controls. From these results, it is assumed that the anticonvulsant effect of bilobalide against convulsions induced by MPN partly involves modulation of hepatic drug-metabolizing enzyme activity, which leads to accelerated elimination of MPN.

Administration, Oral↗

Involvement of tyrosine kinase in capacitative Ca2+ entry pathway in rat glioma C6 cells.

Capacitative Ca2+ entry, a main pathway of Ca2+ entry evoked by receptor activation, is widely confirmed in various types of cells. However, the mechanism of the activation of capacitative Ca2+ entry is unknown. We checked the several candidates for the mechanism of capacitative Ca2+ entry pathway in rat glioma C6 cells using thapsigargin (TG), a microsomal Ca(2+)-ATPase inhibitor. Pretreatment with pertussis toxin did not affect the peak and sustained elevation of [Ca2+]i evoked by TG. Sodium nitroprusside and 8-bromo cyclic GMP did not affect an elevation of [Ca2+]i induced by TG. Phorbol 12-myristate 13-acetate, an activator of protein kinase C (PKC), and staurosporine, an inhibitor of PKC, did not modify an increase in [Ca2+]i induced by TG. Okadaic acid, an inhibitor of phosphatase, did not affect an increase in [Ca2+]i evoked by TG. Pretreatment with colchicine and cytochalasin D, drugs disrupting cytoskeleton, had no effect on a rise of [Ca2+]i induced by TG. Genistein and erbastatin analog, inhibitors of tyrosine kinase, inhibited an elevation of [Ca2+]i evoked by TG in a dose-dependent manner. The present results suggest that tyrosine kinase regulates capacitative Ca2+ entry into rat glioma C6 cells.

Animals↗

Characterization of the contractile response induced by 5-methoxytryptamine in rat stomach fundus strips.

This study examined effects of 5-methoxytryptamine (5-MOT), an agonist at 5-HT4 and 5-HT2B receptors, on the contractile response and acetylcholine release in rat stomach fundus strips. 5-MOT (10(-9)-10(-5) M) produced a concentration-dependent increase in the contraction, while it evoked acetylcholine release in a 'bell-shaped' concentration-dependent manner. Atropine reduced 5-MOT (10(-8)-10(-6) M)-induced contractions, but it had little effect on the contractions evoked by higher concentrations. 5-MOT-induced contraction and acetylcholine release were inhibited by SDZ 205-557 (2-methoxy-4-amino-5-chloro-benzoic acid 2-[diethylamino] ethyl ester), a 5-HT4 receptor antagonist. In the presence of atropine, both SDZ 205-557 and yohimbine, a 5-HT2B receptor antagonist, inhibited the contraction. In the presence of tetrodotoxin, the contraction was inhibited by yohimbine, but not by SDZ 205-557. These results suggest that the contractile action of 5-MOT in rat stomach fundus involves atropine-sensitive and atropine-resistant components. The sensitive contraction appears to be mediated through 5-HT4 receptors located on cholinergic neurons, whereas the resistant contraction is mediated through 5-HT4 receptors located on non-cholinergic neurons and through 5-HT2B receptors.

4-Aminobenzoic Acid↗

Lysophosphatidic acid-sensitive intracellular Ca2+ store does not regulate Ca2+ entry at plasma membrane in Jurkat human T-cells.

In Jurkat T cells, the anti-CD3 antibody OKT3 and thapsigargin (TG) elevated the cytoplasmic free Ca2+ concentration ([Ca2+]i), after which it decreased to a sustained, elevated level. In contrast, lysophosphatidic acid (LPA) increased [Ca2+]i only briefly and transiently, after which it declined to the resting level of [Ca2+]i even in the presence of extracellular Ca2+. OKT3 increased Ins(1,4,5)P3 formation but neither LPA nor TG did. In the absence of extracellular Ca2+, the addition of OKT3 did not affect an elevation of [Ca2+]i induced by the subsequent addition of LPA and vice versa. In permeabilized Jurkat cells, the addition of Ins(1,4,5)P3 released Ca2+; this was inhibited by heparin, whereas LPA released Ca2+ even in the presence of heparin. cADP-ribose released Ca2+; this was additive with LPA-induced Ca2+ release and vice versa in permeabilized Jurkat cells. LPA did not stimulate Ca2+ entry and 45Ca2+ uptake but OKT3 and TG did. LPA, OKT3 and TG did not affect the sustained elevation of [Ca2+]i induced by ionomycin. The present results suggest that at least three kinds of intracellular Ca2+ stores, which are Ins(1,4,5)P3,-cADP-ribose- and LPA-sensitive, exist in Jurkat T cells, and that the LPA-sensitive intracellular Ca2+ store does not regulate Ca2+ entry at the plasma membrane.

CD3 Complex↗

Ca2+ mobilizing action of sphingosine in Jurkat human leukemia T cells. Evidence that sphingosine releases Ca2+ from inositol trisphosphate- and phosphatidic acid-sensitive intracellular stores through a mechanism independent of inositol trisphosphate.

Effects of sphingosine on Ca2+ mobilization in the human Jurkat T cell line were examined. Sphingosine increased the cytoplasmic Ca2+ concentration ([Ca2+]i) in a dose-dependent manner with an ED50 of around 8 microM. Sphingosine and OKT3, a CD3 monoclonal antibody, transiently increased [Ca2+]i, which declined to the resting level in the absence of extracellular Ca2+. Under the same conditions, pretreatment with sphingosine inhibited but did not abolish an increase in [Ca2+]i induced by the subsequent addition of OKT3 and vice versa. However, pretreatment with sphingosine did not affect an increase in [Ca2+]i induced by OKT3 in the presence of Ca2+. OKT3 increased IP3 formation, but sphingosine did not affect the level of IP3 by itself nor did it cause IP3 formation induced by OKT3. In permeabilized Jurkat cells, the addition of IP3 released Ca2+ from nonmitochondrial intracellular stores, but the addition of sphingosine did not. Sphingosine, stearylamine, and psychosine increased [Ca2+]i and diacylglycerol (DG) kinase activation; however, ceramide did not, whereas sphingosine 1-phosphate slightly activated DG kinase without elevation of [Ca2+]i. Pretreatment with R59022, a DG kinase inhibitor, abolished the peak but did not affect the sustained response to [Ca2+]i to sphingosine. Phosphatidic acid (PA) elevated [Ca2+]i, after which it declined to a resting level even in the presence of extracellular Ca2+. In accordance with this, PA did not stimulate 45Ca2+ uptake into cells, but sphingosine and OKT3 did. Pretreatment with PA partially inhibited a rise in [Ca2+]i induced by the subsequent addition of sphingosine and vice versa in the absence of extracellular Ca2+. Under similar conditions, pretreatment with PA affected an elevation of [Ca2+]i induced by OKT3 less, after which the subsequent addition of sphingosine did not increase [Ca2+]i. In permeabilized Jurkat cells, the addition of IP3 did not release Ca2+, but PA did in the presence of heparin. Pretreatment with thapsigargin, a microsomal Ca2+-ATPase inhibitor, abolished the rises of [Ca2+]i induced by the subsequent addition of sphingosine, OKT3, and PA in the absence of extracellular Ca2+. The present results suggest that at least two kinds of intracellular Ca2+ stores exist in Jurkat cells, both of which are IP3- and PA-sensitive, and that sphingosine mobilizes Ca2+ from both stores in an IP3-independent manner. Furthermore, the IP3- but not the PA-sensitive intracellular Ca2+ store seems to regulate Ca2+ entry induced by sphingosine.

Amines↗

Alpha 1- and beta-adrenergic and muscarinic-cholinergic regulation in the spontaneous beating and Ca2+ oscillations in cultured neonatal rat cardiac myocytes.

alpha 1- and beta-adrenergic and muscarinic-cholinergic regulation in spontaneous beating and Ca2+ oscillations in neonatal rat cardiac myocytes at day 6 of culture was investigated. The spontaneous beating in myocytes decreased in the presence of 10 microM norepinephrine (NE). This negative chronotropic action was antagonized by prazosin. Carbachol (CCh) also showed negative chronotropic action which was inhibited by atropine. On the other hand, isoproterenol (ISP) increased the beating rate which was antagonized by propranolol. NE increased inositol phosphate formation whereas CCh and ISP did not. NE and CCh suppressed the frequency of the spontaneous Ca2+ oscillations but ISP increased. The present results suggest that alpha 1-adrenergic and muscarinic receptors regulate chronotropism to be negative whereas beta-adrenoceptor regulates chronotropism to be positive in cultured neonatal rat cardiac myocytes.

Adrenergic Agents↗

Tetrandrine as a calcium antagonist.

1. The Ca(2+)-antagonism of tetrandrine (TET) on the Ca2+ mobilization in various types of cells were reviewed. Inositol trisphosphate (IP3)-generating drugs were used as Ca(2+)-mobilizing agonists and the effects were compared with those produced by using the microsomal Ca(2+)-ATPase inhibitor thapsigargin (TG), which is a tool for analysing Ca2+ store-regulated Ca2+ entry (capacitative Ca2+ entry). 2. In rat phaeochromocytoma PC12 cells, 100 mumol/L TET abolished high K+ (30 mmol/L)-induced sustained increases in cytoplasmic Ca2+ concentrations ([Ca2+]i) and partially inhibited bradykinin (1 mumol/L)- or TG (100 nmol/L)-induced Ca2+ entry. 3. In NIH/3T3 fibroblasts and rat parotid acinar cells, 100 mumol/L TET abolished Ca2+ entry induced by bombesin (1 mumol/L) and carbachol (100 mumol/L), respectively, or TG (100 nmol/L). However, in the human leukaemia T cell line Jurkat, 100 mumol/L TET did not inhibit Ca2+ entry evoked by either the anti-CD3 antibody OKT3 (10 mg/L) or TG (100 nmol/L). 4. In rat glioma C6 cells, the effects of TET on Ca2+ mobilization were further examined. At a high concentration, TET (300 mumol/L) alone did not affect [Ca2+]i in C6 cells. Tetrandrine inhibited the peak and sustained increases in [Ca2+]i induced by bombesin and TG in a dose-dependent manner. Although TET or TG did not produce increases in IP3, TET did inhibit increases in IP3 produced by bombesin. 5. Our results suggest that the action of TET on Ca2+ entry is dependent on cell types and that TET inhibits both Ca2+ entry from the extracellular medium and Ca2+ release from intracellular stores in rat glioma C6 cells.

Alkaloids↗

Role of L-type calcium channels on halothane-induced myocardial depression in cultured rat ventricular myocytes.

The effects of antagonists for L-type Ca2+ channel, opener and blocker to ATP-sensitive K+ (KATP) channel, phosphodiesterase inhibitor, or Ca2+ sensitizer on halothane-induced myocardial depression were investigated in cultured rat ventricular myocytes. Halothane (1 to 4%) decreased the beating rate and amplitude in a dose-dependent manner. Myocardial depressant effects of halothane were potentiated by the presence of 10 nM nifedipine or verapamil. Neither cromakalim (1 microM), glibenclamide (1 microM), nor pimobendan (10 microM) altered the dose-dependent depressant effects of halothane. The mechanisms involving altered KATP channel, cAMP levels or Ca2+ sensitivity of contractile proteins may not be responsible for myocardial depression during halothane exposure. These results suggest that changes in L-type Ca2+ channel function plays an important role in the volatile anesthetic halothane-induced depression of contractile activity in cultured rat ventricular myocytes.

Anesthetics, Inhalation↗

Lack of voltage-operated calcium channel in rat glioma C6 cells.

We examined whether rat glioma C6 cells have voltage-operated Ca2+ channel (VOC) or not. The addition of high K+ did not affect the cytoplasmic Ca2+ concentration ([Ca2+]i). In addition, BAY K 8644, a VOC against, did not increase [Ca2+]i even in the presence of high K+. Bombesin (BBS), an inositol trisphosphate-generating drug, and thapsigargin (TG), a microsomal Ca(2+)-ATPase inhibitor, increased [Ca2+]i, after which it decreased to a sustained, and still higher than original level. The addition of verapamil, diltiazem and nimodipine did not affect an increase in [Ca2+]i induced by BBS and TG. The addition of SK&F 96365, a receptor-operated Ca2+ channel (ROC) blocker, reduced the sustained increase in [Ca2+]i induced by BBS and TG. The present results suggest that VOC does not exist in rat glioma C6 cells and this cell line is a good model for investigating signal transduction via ROC as glial cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗