Biomedical subjects

Y F Xu

Publications and source records attributed to Y F Xu.

At least 19 recordsLinked to original sources

PubMed2006

Research on inhibitive behaviors of electrolysis on the growth of Microcystis aeruginosa.

Electrochemical method using a novel Ti/RuO2 anode was employed to inhibit a typical cyanobacteria, Microcystis aeruginosa (M. aeruginosa) under different electrolytic conditions. It is demonstrated that Ti/RuO2 anode was more efficient than traditional graphite anode in M. aeruginosa inhibition. The experimental results showed that the higher current density or longer electrolytic time could effectively improve the inhibition of M. aeruginosa. In addition, sodium chloride was a more effective electrolyte than sodium sulfate to enhance inhibition. The maximum inhibiting rate dose to 100% could be obtained at a current density of 12 mA cm(-2) when sodium chloride was used as a supporting electrolyte. Furthermore, UV-Visible spectra demonstrated that the structures of phycocyanins and chlorophyll a (Chl a) in M. aeruginosa could be changed or destroyed during electrolysis. Moreover, EPR spectra showed the generation of the free radicals through electrolysis, which might be one of the reasons responsible for the inhibition of algal growth.

Chlorophyll↗

PubMed2005

Possible association of the MAG locus with schizophrenia in a Chinese Han cohort of family trios.

Neurotransmitter-based hypotheses have so far led to only moderate success in predicting new pathogenetic findings in etiology of schizophrenia. On the other hand, the more recent oligodendroglia hypotheses of this disorder have been supported by an increasing body of evidence. For example, the expression level of the myelin associated glycoprotein (MAG) gene has been shown to be significantly lower in schizophrenia patient groups compared to control groups. Such an effect might be a result of genetic variations of the MAG gene. In order to test this hypothesis, we genotyped four markers within the MAG locus in 413 trios sample of the Han Chinese using allele-specific PCR. None of the four markers revealed noticeable allelic significance. However, the four-marker and two-marker haplotypes covering components rs720309 and rs720308 were observed to be significantly associated with schizophrenia (P < 0.0001) in this study. In addition, we identified one common risk haplotype TA (rs720309-rs720308, present in 78.5% of the general population) that showed increased evidence of overtransmission from parents to affected offspring (P = 0.0001). The results demonstrated MAG might play a role in genetic susceptibility to schizophrenia. Furthermore, our finding of a possible association between the MAG locus and schizophrenia is in agreement with the hypotheses of oligodendrltic and myelination dysfunction.

Adult↗

PubMed2005

Quantitative analysis of the response of an electrochemical biosensor for progesterone in milk.

An electrochemical biosensor for progesterone in cow's milk was developed and used in a competitive immunoassay by Hart et al. (1977, Studies towards a disposable screenprinted amperometric biosensor for progesterone, Biosens. Bioelectron. 12, 1113-1121). The sensor was fabricated by depositing anti-progesterone monoclonal antibody (mAb) onto screen-printed carbon electrodes (SPCEs) which were coated with rabbit anti-sheep IgG (rIgG). This sensor was operated following the steps of competitive binding between sample and conjugate (alkaline-phosphatase-labelled progesterone) for the immobilised mAb sites and measurements of an amperometric signal in the presence of p-nitrophenylphosphate using either colorimetric assays or cyclic voltammetry. The hook effect of the progesterone biosensor was found in the concentration range of milk progesterone between 0 and 5 ng/ml when the sensor was fabricated using a loading of 25 ng rIgG per electrode of a diameter of 3 mm and a 1/50 dilution of mAb. A computer model has been developed in this study to simulate the operation of this progesterone biosensor with consideration of the fabrication processes. This paper presents the results of validating the computer model and the model has predicted the hook effect as observed in tests. The model thus reveals that the hook effect is determined by the total number of binding sites available and the rates of labelled and unlabelled progesterone diffusing towards the sensor surface and the binding rates.

Animals↗

PubMed2005

The tumor suppressor adenomatous polyposis coli gene is associated with susceptibility to schizophrenia.

The etiology of schizophrenia is unclear, although family, twin, and linkage studies implicate genetic factors. Here, we identified adenomatous polyposis coli (APC), a tumor suppressor gene, as a risk factor for schizophrenia. We compared leukocytic gene expression patterns of six pairs of patients with schizophrenia and healthy controls by microarray. APC expression levels were significantly increased in all patients compared to healthy controls. To confirm the findings of microarray analysis, we measured expression levels of APC in the leukocytes from 30 relapse patients taking antipsychotic medication, 29 first-episode drug-naïve patients, and 30 healthy controls using real-time quantitative reverse transcription (RT)-polymerase chain reaction (PCR). APC expression levels were significantly increased in leukocytes of schizophrenics both taking and not taking antipsychotic medication and hence the increase of APC expression was not due to antipsychotic medication. APC is located at 5q21-22, which has been previously reported to be linked with schizophrenia. Further, we performed the transmission disequilibrium test (TDT) and TDT based on haplotypes to search for the association between schizophrenia and APC by examining 163 parent-offspring trios of Chinese descent. We analyzed three single-nucleotide polymorphisms (SNPs) (rs2229992, rs42427, rs465899) at the exon region of APC. TDT showed that the three SNPs are significantly associated with schizophrenia (TDT chi(2)=4.23, P<0.05; 4.15, P<0.05; 8.49 P<0.01, respectively; HHRRchi(2)=5.54, P<0.05; 4.40, P<0.05; 9.79, P<0.01, respectively). We found a significant association between the APC haplotypes from rs2229992-rs42427-rs465899 and schizophrenia (Global chi(2)=44.376,df=7, P<0.001). The C-A-T haplotype has a frequency of more than 57% and has a strong association with schizophrenia (chi(2)=15.04, P<0.001). These results indicate that the APC may be a candidate gene conferring susceptibility to schizophrenia and also may be associated with reduced vulnerability to cancer in schizophrenia.

Adenomatous Polyposis Coli Protein↗

PubMed2000

[Role of calcineurin in cardiac fibroblast proliferation stimulated by angiotensin II].

The present study was undertaken to observe the role of calcineurin (CaN) in the angiotensin II (Ang II) stimulated cardiac fibroblast proliferation. In cultured cardiac fibroblasts of neonatal rats, Ang II was used to stimulate proliferation while CaN was inhibited by CaN CsA inhibitor cyclosporin A (CsA). (3)H-TdR incorporation, activity of CaN and intracellular calcium concentration were measured. (3)H-TdR incorporation of Ang II stimulated fibroblasts was 72% higher than control (P<0.01), which was inhibited by CsA (0.1 10 micromol/L) in a dose dependent manner. Intracellular Ca(2+) level and CaN activity of Ang II stimulated fibroblasts were respectively 112% (P<0.01) and 17%(P<0.05) higher than control. It is concluded that CaN may play an important role in signal transduction of the Ang II induced cardiac fibroblast proliferation.

Angiotensin II↗

PubMed1999

Effect of moxonidine on carotid sinus baroreflex in anesthetized rats.

AIM: To study the effect of moxonidine (Mox) on carotid sinus baroreflex. METHODS: By perfusing the carotid sinus in anesthetized rats, the functional parameters of baroreflex were measured. The femoral artery was perfused with constant flow and the change of perfusing pressure was recorded to determine the effect of Mox on vascular tone. RESULTS: Mox 32 and 100 mumol.L-1 shifted the functional curve of carotid sinus baroreflex to the right and upward, with the reduction in peak slope and in reflex decrease of mean arterial pressure, suggesting that Mox produced an inhibitory effect on baroreflex. The effect of Mox 100 mumol.L-1 on baroreflex was completely blocked by efaroxan 100 mumol.L-1. Mox increased vascular resistance. CONCLUSION: Mox inhibits carotid baroreflex via its constrictive action on sinus wall.

Adrenergic alpha-Antagonists↗

PubMed1998

Passive transfer of Lambert-Eaton myasthenic syndrome induces dihydropyridine sensitivity of ICa in mouse motor nerve terminals.

Mice were injected for 30 days with plasma from three patients with Lambert-Eaton Myasthenic Syndrome (LEMS). Recordings were made from the perineurial sheath of motor axon terminals of triangularis sterni muscle preparations. The objective was to characterize pharmacologically the identity of kinetically distinct, defined potential changes associated with motor nerve terminal Ca2+ currents (ICa) that were affected by LEMS autoantibodies. ICa elicited at 0.01 Hz were significantly reduced in amplitude by approximately 35% of control in LEMS-treated nerve terminals. During 10-Hz stimulation, ICa amplitude was unchanged in LEMS-treated motor nerve terminals, but was depressed in control. During 20- or 100-Hz trains, facilitation of ICa occurred in LEMS-treated nerve terminals whereas in control, no facilitation occurred during the trains at 20 Hz and marked depression occurred at 100 Hz. Saturation for amplitude and duration of ICa in control terminals occurred at 2 and 4-6 mM extracellular Ca2+, respectively; in LEMS-treated terminals, the extracellular Ca2+ concentration had to increase by two to three times of control to cause saturation. Amplitude of the two components of ICa observed when the preparation was exposed to 50 microM 3,4-diaminopyridine and 1 mM tetraethylammonium were both reduced by LEMS plasma treatment. The fast component (ICa,s) was reduced by 35%, whereas the slow component (ICa, s) was reduced by 37%. omega-Agatoxin IVA (omega-Aga-IVA; 0.15 microM) and omega-conotoxin-MVIIC (omega-CTx-MVIIC; 5 microM) completely blocked ICa in control motor nerve terminals. The same concentrations of toxins were 20-30% less effective in blocking ICa in LEMS-treated terminals. The residual ICa remaining after treatment with omega-Aga-IVA or omega-CTx-MVIIC was blocked by 10 microM nifedipine and 10 microM Cd2+. Thus LEMS plasma appears to downregulate omega-Aga-IVA-sensitive (P-type) and/or omega-CTx-MVIIC-sensitive (Q-type) Ca2+ channels in murine motor nerve terminals, whereas dihydropyridine (DHP)-sensitive (L-type) Ca2+ channels are unmasked in these terminals. Acute exposure (90 min) of rat forebrain synaptosomes to LEMS immunoglobulins (Igs; 4 mg/ml) did not alter the binding of [3H]-nitrendipine or [125I]-omega-conotoxin-GVIA (-omega-CgTx GVIA) when compared with synaptosomes incubated with an equivalent concentration of control Igs. Conversely, LEMS Igs significantly decreased the Bmax for [3H]-verapamil to approximately 45% of control. The apparent affinity of verapamil (KD) for the remaining receptors was not significantly altered. Thus acute exposure of isolated central nerve terminals to LEMS Igs does not increase DHP sensitivity, whereas it reduces the number of binding sites for verapamil but not for nitrendipine or omega-CgTx-GVIA. These results suggest that chronic but not acute exposure to LEMS Igs either upregulates or unmasks DHP-sensitive Ca2+ channels in motor nerve endings.

Animals↗

PubMed1998

[Isolation of novel expression sequences of C2H2 type zinc finger protein gene from human brain tissue according to the conservation of zinc finger motif].

By low stringency PCR amplification of genomic DNA using the primers designed based on the conservation of zinc finger motif, we got 8 gradient eletrophoretic bands. After recovery of the second and third bands, the DNA fragments in them were cloned and sequenced. Compared to the GenBank database, among these 60 segments containing zinc finger motif, 23 segments were novel zinc finger genes' genomic segments. Then the human brain tissue cDNA library was screened, using these segments as probes, and 44 positive clones were obtained. Rescreening 28 of them, we got 20 rescreened clones. All of them were sequenced and sent to the GenBank DNA database for sequence analysis, the results showed that 16 were novel C2H2 type zinc finger protein cDNA segments. The cDNA segments encoding the novel C2H2 type zinc finger proteins provide the basic materials for cloning of full length cDNA of valuable novel zinc finger protein genes.

Amino Acid Sequence↗

PubMed1997

Effects of moxonidine injected into rostral ventrolateral medulla on blood pressure, heart rate, and renal sympathetic nerve activity in rats.

AIM: To examine the effects of moxonidine (Mox) injected into the rostral ventrolateral medulla (RVLM) on blood pressure (BP), heart rate (HR), and the renal sympathetic nerve activity (RSNA) in anesthetized normotensive rats. METHODS: BP, HR, and RSNA were simultaneously recorded after 1 microL Mox 1, 10, and 100 mumol.L-1 was injected into RVLM. RESULTS: Mox 1, 10, and 100 mumol.L-1 reduced BP from 13.9 +/- 1.0 kPa to 13.0 +/- 1.7 kPa (P < 0.05), 13.8 +/- 1.8 kPa to 11.4 +/- 1.5 kPa (P < 0.01), and 13.9 +/- 1.9 kPa to 9.4 +/- 1.7 kPa (P < 0.01), respectively. Mox did not influence HR. RSNA varied with the doses: Mox 1 mumol.L-1 increased RSNA by 50% (P < 0.05), 10 mumol.L-1 insignificantly influenced RSNA (P > 0.05), and 100 mumol.L-1 reduced RSNA by 23% (P < 0.05). In sinoaortic barodenervated rats, Mox 10 mumol.L-1 inhibited RSNA by 50% (P < 0.05), which substantially differed from that in buffer nerve intact rats (P < 0.01). CONCLUSION: Mox injected into RVLM decreased BP, but did not influence HR. The changes of RSNA did not parallel with the depressor effect of Mox.

Animals↗

PubMed1996

Effects of omega-agatoxin-IVA and omega-conotoxin-MVIIC on perineurial Ca++ and Ca(++)-activated K+ currents of mouse motor nerve terminals.

Effects of omega-agatoxin-IVA (omega-Aga-IVA) and omega-conotoxin-MVIIC (omega-CTx-MVIIC) on mouse motor nerve terminal Ca+2 currents and Ca(+2)-activated K+ currents (IK,Ca) were compared using the triangularis sterni preparation and perineurial recording techniques. omega-Aga-IVA caused concentration- and time-dependent block of both the fast (ICa-f) and slow (ICa-s) components of Ca+2 current. Low concentrations (10 nM) caused preferential block of ICa-s. Higher concentrations (100-150 nM) of omega-Aga-IVA blocked ICa-f effectively. omega-CTx-MVIIC blocked both ICa-s and ICa-f with equal sensitivity; however, higher concentrations and longer exposure times than those required for omega-Aga-IVA were needed. omega-CTx-MVIIC could block the residual ICa-f that remained after pretreatment with Cd+2 or omega-Aga-IVA. Increasing the extracellular Ca+2 concentration partially antagonized the effects of both omega-Aga-IVA and omega-CTx-MVIIC on ICa-s and ICa-f. Washing the preparation with toxin-free solution only slightly antagonized the effect of omega-Aga-IVA and was ineffective in omega-CTx-MVIIC-treated preparations. Low concentrations of omega-Aga-IVA and omega-CTx-MVIIC increased the duration of IK,Ca whereas higher concentrations reduced the amplitude of IK,Ca. Thus, at mouse motor nerve terminals, both omega-Aga-IVA- and omega-CTx-MVIIC-sensitive Ca+2 currents exist. omega-Aga-IVA appears to be more selective in blocking nerve terminal Ca+2 current than does omega-CTx-MVIIC. Paradoxically, block of ICa-s alone by omega-Aga-IVA and, to a lesser extent, omega-CTx-MVIIC was associated with increased duration of IK,Ca whereas block of ICa-s and ICa-f by omega-Aga-IVA and omega-CTx-MVIIC was associated with reduced amplitude of IK,Ca.

Action Potentials↗

PubMed1995

Multidrug resistance in leukemic cell line K562/A02 induced by doxorubicin.

AIM: To study the mechanism of the development of multidrug resistance in leukemic cells. METHODS: A human leukemic cell line K562/A02 was established by stepwise increase of concentrations of doxorubicin (Dox) in medium. P-glycoprotein was detected by immunohistochemistry assay. The mdr1 gene expression was measured by RT-PCR. The amplification of mdr1 gene in its genome, and DNA topisomerase II (Top II) gene expression were determined by dot-blot hybridization. RESULTS: K562/A02 was highly cross-resistant to vincristine (VCR), homoharringtonin (HHT), amsacrine (m-AMSA), daunorubicin (Dau) and etoposide (VP-16), slightly to cytosine arabinoside (Ara-C), but not cisplatin (Cis), methotrexate (MTX) and fluorouracil (5-FU), showing a typical phenotype of MDR. Intracellular accumulation of Dau in K562/A02 was 33% as high as that in K562. P-glycoprotein P-170 was positive. In K562/A02, the mdr1 gene did not amplify, the mdr1 mRNA level was markedly higher, the Top II mRNA level was lower, and glutathione-S-transferase (GST) activity was higher than in K562. CONCLUSION: mdr1 mRNA was overexpression and thus the encoded P-170 was responsible for MDR in K562/A02 while Top II or GST may play a role in MDR.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1995

[Reversible elimination of K+ and Na+ currents at motor nerve terminals by SM486, a derivative of artemisinin].

Some derivatives of Artemisinin have been used as malariacides. Artemisinin derivative SM486 is water-soluble and has been shown also to have local anesthesia action. Here we report the effect of SM486 on Na+ and K+ channels at motor nerve terminals. Experiments were performed on mouse triangularis sterni nerve-muscle preparations. Presynaptic currents were picked up with a microelectrode inserted into the subendothelial space of the superficial nerve bundle under visual control using a x400 magnification water immersion objective. The results showed: (1) Both IK and INa were depressed in a dose-dependent manner, although the minimal effective concentration of SM486 for IK was lower than that for INa; (2) The depression was reversible as shown by the fact that the nearly completely blocked INa and IK currents could be restored to the control by simply washing away the perfusate SM486. (3) The decrease of IK was progressive, while the change of INa always began after IK proceeded to decrease rapidly. The effects of procaine on INa and IK are similar to SM486 but the effective concentration was higher.

Anesthetics, Local↗

PubMed1994

Plasmenylcholine (1-O-alk-1'-enyl-2-acyl-sn-glycero-3-phosphocholine) biosynthesis in guinea-pig heart and liver: cholinephosphotransferase is a bifunctional enzyme for the synthesis of phosphatidylcholine and plasmenylcholine.

Plasmenylcholine is present in significant proportion (32% of choline phosphoglycerides) in the guinea-pig heart but exists as a minor component (3% of choline phosphoglycerides) in the guinea-pig liver. In this study, the biosynthesis of plasmenylcholine in these two organs was examined. The organs were perfused with labelled choline for 15 min and chased with unlabelled choline for up to 7 h. The labelling of phosphatidylcholine was 6-fold higher than that of plasmenylcholine in the heart and about 60-fold higher in the liver. However, the same labelling ratio was maintained throughout the chase period in both organs. Alterations in the specific radioactivity of CDP-choline caused corresponding changes in the labelling of phosphatidylcholine and plasmenylcholine. Our results suggest that in guinea-pig heart and liver, CDP-choline is the immediate precursor of biosynthesis of phosphatidylcholine and plasmenylcholine. The biochemical cause for the difference in their rates of formation between the two organs was explored. The enzyme activities for the formation of both choline phosphoglycerides were determined. The two reactions share the same characteristics, and 1,2-diacylglycerol and 1-alk-1'-enyl-2-acylglcerol were found to be mutually inhibitory in a competitive fashion. The pool sizes of 1,2-diacylglycerol and 1-alk-1'-enyl-2-acylglycerol were determined, and their ratios were found to be 42 in the heart and 422 in the liver. We conclude that cholinephosphotransferase catalyses the formation of both phosphatidylcholine and plasmenylcholine in the guinea-pig tissues and the rate of plasmenylcholine biosynthesis is dependent on the availability of 1-alk-1'-enyl-2-acylglycerol. Plasmenylcholine biosynthesis is also subjected to modulation by the 1,2-diacylglycerol content of the tissue.

Animals↗

PubMed1994

Cellular transformation by a transmembrane peptide: structural requirements for the bovine papillomavirus E5 oncoprotein.

The E5 oncoprotein of bovine papillomavirus, only 44 amino acids long, occurs as a disulfide-bonded transmembrane dimer. This remarkable oncoprotein stimulates signal transduction through activation of the platelet-derived growth factor (PDGF) receptor, and E5 exhibits limited amino acid sequence similarity with PDGF. Results presented here suggest that a key feature of the hydrophobic transmembrane domain is an amino acid side chain that participates in interhelical hydrogen bond formation. These data are reminiscent of the activated neu oncogene, in which a point mutation in the transmembrane domain leads to ligand-independent dimerization and activation of a receptor tyrosine kinase. Significantly, the transmembrane domain of E5 can be largely replaced by the transmembrane domain from the activated neu receptor tyrosine kinase. Extensive mutagenesis defines the minimal structural features required for transformation by the E5 oncoprotein as, first, the ability to dimerize and, second, presentation of a negatively charged residue at the extracellular side of the membrane. The biological activity of E5 mutants that lack most amino acid residues similar to PDGF suggests that E5 and PDGF activate the PDGF receptor by distinct mechanisms.

Amino Acid Sequence↗

PubMed1994

The v-sis oncoprotein loses transforming activity when targeted to the early Golgi complex.

The location of autocrine interactions between the v-sis protein and PDGF receptors remains uncertain and controversial. To examine whether receptor-ligand interactions can occur intracellularly, we have constructed fusion proteins that anchor v-sis to specific intracellular membranes. Fusion of a cis-Golgi retention signal from a coronavirus E1 glycoprotein to v-sis protein completely abolished its transforming ability when transfected into NIH3T3 cells. Fusion proteins incorporating mutations in this retention signal were not retained within the Golgi complex but instead were transported to the cell surface, resulting in efficient transformation. All chimeric proteins were shown to dimerize properly. Derivatives of some of these constructs were also constructed bearing the cytoplasmic tail from the glycoprotein of vesicular stomatitis virus (VSV-G). These constructs allowed examination of subcellular localization by double-label immunofluorescence, using antibodies that distinguish between the extracellular PDGF-related domain and the VSV-G cytoplasmic tail. Colocalization of sis-E1-G with Golgi markers confirmed its targeting to the early Golgi complex. The sis-E1 constructs, targeted to the early Golgi complex, exhibited no proteolytic processing whereas the mutant forms of sis-E1 exhibited normal proteolytic processing. Treatment with suramin, a polyanionic compound that disrupts ligand/receptor interactions at the cell surface, was able to revert the transformed phenotype induced by the mutant sis-E1 constructs described here. Our results demonstrate that autocrine interactions between the v-sis oncoprotein and PDGF receptors within the early Golgi complex do not result in functional signal transduction. Another v-sis fusion protein was constructed by attaching the transmembrane domain and COOH-terminus of TGN38, a protein that localizes to the trans-Golgi network (TGN). This construct was primarily retained intracellularly, although some of the fusion protein reached the surface. Deletion of the COOH-terminal region of the TGN38 retention signal abrogated the TGN-localization, as evidenced by very prominent cell surface localization, and resulted in increased transforming activity. The behavior of the sis-TGN38 derivatives is discussed within the context of the properties of TGN38 itself, which is known to recycle from the cell surface to the TGN.

3T3 Cells↗

PubMed1994

The A and B isoforms of the human progesterone receptor operate through distinct signaling pathways within target cells.

The biological response to progesterone is mediated by two distinct forms of the human progesterone receptor (hPR-A and hPR-B). In most cell contexts, hPR-B functions as a transcriptional activator of progesterone-responsive genes, whereas hPR-A functions as a transcriptional inhibitor of all steroid hormone receptors. We have created mutations within the carboxyl terminus of hPR which differentially effect the transcriptional activity of hPR-B in a cell- and promoter-specific manner. Analogous mutations, when introduced into hPR-A, have no effect on its ability to inhibit the transcriptional activity of other steroid hormone receptors. The observed differences in the structural requirements for hPR-B and hPR-A function suggest that transcriptional activation and repression by PR are mediated by two separate pathways within the cell. In support of this hypothesis, we have shown that hPR-A mediated repression of human estrogen receptor (hER) transcriptional activity is not dependent on hER expression level but depends largely on the absolute expression level of hPR-A. Thus, it appears that hPR-A inhibits hER transcriptional activity as a consequence of a noncompetitive interaction of hPR-A with either distinct cellular targets or different contact sites on the same target. We propose that hPR-A expression facilitates a ligand-dependent cross-talk among sex steroid receptor signaling pathways within the cell. It is likely, therefore, that alterations in the expression level of hPR-A or its cellular target can have profound effects on the physiological or pharmacological responses to sex steroid hormone receptor ligands.

Base Sequence↗

PubMed1994

Effects of inhibitor of endothelium-derived relaxing factor on hypoxic contraction of isolated pig coronary artery.

Exposure of isolated pig coronary artery with endothelium intact to hypoxia Krebs-Henseleit solution aerated with 95% N2 + 5% CO2 caused a transient contractile response, and the coronary artery without endothelium exhibited a gradual decrease in basal tension. The endothelium-dependent contractile response to hypoxia was almost completely blocked by nitro-L-arginine (0.2 mmol.L-1), and inhibited by methylthioninium chloride (10 mumol.L-1). The inhibitory effect of the NLA was partially reversed by L-arginine (2 mmol.L-1). Sodium nitroprusside (10 mumol.L-1) was also completely antagonized and nicorandil (0.3 mol.L-1) remarkably reduced the hypoxic contractile response. Tetraethylammonium (10 mmol.L-1) and glibenclamide (1 mumol.L-1) had little effect on hypoxia-induced vascular contraction, whereas cromakalim (1 mumol.L-1) produced obvious relaxing effect on hypoxic response. These results suggest that suppression of basally released nitric oxide (NO) is an important mechanism of coronary vasoconstriction induced by hypoxia.

Animals↗

PubMed1994

Effect of Pinellia ternata lectin on membrane currents of mouse motor nerve terminals.

Pinellia ternata lectin (PTL) extracted from the fresh juice of rhizome of pinellia ternata used as a traditional Chinese medicine facilitated the quantal release of acetylcholine (ACh) in the mouse motor nerve terminals and formed cation channels in artificial lipid bilayer. Here we report the action of PTL on presynaptic membrane currents of motor nerve terminals. The experiments were performed on the intercostal nerve triangularis sterni muscle preparations. By means of the perineurial recording, the effects of PTL on the sodium current in the preterminal part, three potassium currents and two calcium currents generated from the nerve terminals were investigated. The results show that PTL increases voltage-dependent fast Ca2+ current (ICa.f), Na+ current (INa) and Ca(2+)-activated K+ current (IK,Ca) without action on either the voltage-dependent fast K+ current (IK,f) or the slow K+ current (IK,s). These effects are irreversible, but can be reversed by mannan, the specific binding sugar for PTL. The total action of PTL can be considered to raise [Ca2+]i by promoting Ca2+ influx, and then facilitate the neurotransmitter release. To our knowledge, this is the first report about the influence of lectin on presynaptic membrane currents at mammalian motor nerve terminals.

Animals↗