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Biomedical subjects

Z Zeng

Publications and source records attributed to Z Zeng.

At least 91 records · Page 5Linked to original sources

Tetramethylpyrazine, a Chinese drug, blocks coronary vasoconstriction by endothelin-1 and decreases plasma endothelin-1 levels in experimental animals.

The purpose of this study was to investigate effects of tetramethylpyrazine (TMP), a Chinese plant-derived medicine, on coronary vasoconstriction and related electrocardiographic and histologic changes caused by endothelin-1 (ET-1), and on plasma ET-1 levels. ET-1 (75 pmol) was administered into the left coronary artery (LCA) in anesthetized closed-chest dogs with and without prior infusion of TMP (80 mg/kg). Coronary arterial diameter (CAD) was determined by coronary arteriography (CAG). Blood pressure and electrocardiogram (ECG) were monitored continuously. Histologic damage in tissues was ascertained microscopically. Plasma ET-1 and 6-keto-PGF1 levels were determined by RIA 90 min after i.v. injection of TMP (25 mg/kg; n = 5) in rabbits. Intracoronary injection of ET-1 resulted in a significant vasoconstriction of the entire vascular bed of the LCA, with a decrease in CAD of 35.9 +/- 5.7% (n = 5; p < 0.01) and ischemic changes on ECG and in tissues of endocardium, myocardium, coronary endothelial cells, and capillary vessels. Pretreatment with TMP produced a significant increase in CAD by 38.5 +/- 7.8% (n = 5; p < 0.01) and greatly suppressed the vasoconstriction produced by ET-1. The myocardial tissue damage estimated from the ratio of ischemic area for the entire area after ET-1 injection (35.6%) was completely abolished by TMP (0.6%). In addition, TMP injection induced a significant decrease in plasma ET-1 levels and an increase in 6-keto-PGF1 levels in rabbits. The Chinese medicine TMP could be a useful therapeutic agent in ischemic heart disease by suppressing coronary vasoconstriction and ischemic changes in the tissues produced by ET-1.

6-Ketoprostaglandin F1 alpha↗

Effects of tetramethylpyrazine, a Chinese medicine, on plasma endothelin-1 levels during acute pulmonary hypoxia in anesthetized dogs.

Our study was designed to elucidate the effects of tetramethylpyrazine (TMP), a Chinese medicine, on plasma endothelin-1 (ET-1) levels in dogs with acute pulmonary alveolar hypoxia. Anesthetized dogs were used under artificial ventilation with room air or a hypoxic gas mixture (10% O2 and 90% N2) (n = 10) for 60 min. Effects of TMP (80 mg/kg) were studied by i.v. injection of TMP before exposure to hypoxia (n = 8). Mean pulmonary arterial pressure (PAPm), systemic arterial pressure (SAPm), right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and heart rate (HR) were measured. The pulmonary vascular resistance (PVR) was calculated by the equation of (PAPm-PCWP) x 8/CO. Plasma ET-1 levels were determined in the abdominal aorta and pulmonary artery by RIA. The effects of TMP on PAP and plasma ET-1 level were evaluated by using percent increase in PAPm and the change of Da-pET (delta ET) before and after hypoxia. Both PAPm and PVR were significantly elevated 5 min after acute hypoxia over a period of 60 min, whereas CO and PCWP did not change. Plasma ET-1 levels in the abdominal aorta and Da-pET showed a significant increase. Administration of TMP significantly decreased the hypoxia-induced increase in the PAPm, PVR, and delta ET. These results suggest that TMP could be a useful therapeutic agent in the treatment of pulmonary hypertension induced by acute hypoxia through decrease of plasma ET-1 levels.

Anesthesia, General↗

Haematopoietic action of flt3 ligand on cord blood-derived CD34-positive cells expressing different levels of flt3 or c-kit tyrosine kinase receptor: comparison with stem cell factor.

We compared the effect of human flt3 ligand (FL) and stem cell factor (SCF) on cord blood (CB)-derived CD34+ cells expressing different levels of flt3 or c-kit tyrosine kinase (TK) receptor in clonal cell culture. The c-kit receptor was expressed by 58.5+/-16.7% of CB CD34+ cells (n=19), in which c-kit(high), c-kit(low) and c-kit cell populations could be identified. In contrast, the flt3 receptor (FR) was weakly expressed on 58.6+/-8.3% (n=9) of CB CD34+ cells. FL+erythropoietin (Epo) failed to support erythroid burst (BFU-E) formation by any subpopulation of CD34+ cells. However, SCF + Epo supported BFU-E and erythrocyte-containing mixed (CFU-mix) colony formation from all subpopulations. Interestingly, FL markedly augmented CFU-mix colony formation supported by interleukin (IL)-3 + Epo when CD34+c-kit(low) or CD34+FR+ cells were used as the target. On the other hand, SCF significantly enhanced CFU-mix colony formation supported by IL-3 + Epo when CD34+c-kit(high) or low and CD34+FR+ cells were used. The replating potential of CFU-mix supported by IL-3 + Epo+ FL was greater when CD34+c-kit(low) or CD34+FR+ cells were used. When the CD34+c-kit(low) cells were used, the number of lineages expressed in secondary cultures of CFU-mix colonies derived from primary cultures containing IL-3 + Epo + FL or SCF was significantly larger than when the primary cultures contained IL-3 + Epo. Furthermore, the number of long-term culture-initiating cells found in CD34+FR+ cells was larger than that in FR cells. CB-derived CD34+c-kit(low) cells represent a less mature population than c-kit(high) cells, as reported previously. Therefore, these results indicate that both FL and SCF can act on primitive multipotential progenitors. However, it is still uncertain whether CB-derived CD34+FR+ cells are less mature than CD34+FR- cells.

Antigens, CD34↗

The relatively high frequency of p53 gene mutations in multiple and malignant phaeochromocytomas.

To explore the clinical significance of p53 in the pathogenesis of adrenal neoplasms, we investigated the incidence of p53 gene mutations in functioning human adrenal tumours using the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) technique to screen p53 exons 4 to 9. We examined 29 adrenocortical adenomas (primary aldosteronism, n=17; Cushing's syndrome, n=12, all benign), and 33 phaeochromocytomas (benign solitary, n=18; benign multiple, n=5; malignant, n=10) in Japanese and Chinese patients. PCR-SSCP did not show any abnormal band-shifts in any of the adrenocortical adenoma and benign solitary phaeochromocytoma tissues. In contrast, six phaeochromocytoma tissues (two cases benign multiple, four cases malignant) showed PCR-SSCP band-shifts. Subsequent DNA sequencing analysis of the shifted bands revealed six cases with nine mutations or intronic sequence alterations: three cases contained sequence alterations within intronic regions, three cases with silent mutation (sequence alteration in codon without amino acid alteration), and three cases contained missense mutations (one case each in exons 5, 6 and 9). Immunohistochemical staining demonstrated that two of three cases with missense mutations and one case with an intronic sequence alteration over-expressed p53 protein in tumour cell nuclei. We observed no association between p53 gene mutation and p21/WAF1/Cip-1 expression. The relatively high incidence of p53 gene mutations or intronic sequence alteration in multiple and malignant phaeochromocytomas, but not in benign solitary cases, suggests that p53 mutation could play some role in the pathogenesis of multiple and/or malignant phaeochromocytomas.

Adenoma↗

[Development of mouse and rat model of Helicobacter pylori infection].

OBJECTIVE: To develop different rodent model of H. pylori infection as to meet different requirement for different purpose of study. METHODS: 40 two-grade Wistar rats, 40 two-grade C57BL/6 mice and 40 SPF BALB/c mice were randomly divided into two groups: experimental and control groups. Animals in the experimental group were inoculated orally Hp strain (Sydney Strain 1, SS1), 0.4 ml of inoculum per mouse, 1.5 ml per rat (10(9) organisms/ml) five times for a week. In 4, 8, 12 and 24 weeks after the last bacteria inoculum, 5 animals in the experimental and control groups were sacrificed respectively. Histology and Hp colonization were assessed by HE staining, Gimesa staining, Urease test, and Hp culture. RESULTS: In 4 weeks, in all experimental animals bacteria were clearly visible at antrum and body, but the number of Hp colonization varied according to the animal strain. Heavy colonization was seen in C57BL/6 in antrum and body, and in BALB/c and Wistar colonization was located mainly at antrum, less at body, which tended to increase over the experiment time, especially in Wistar. Hp was negative in the controls. All animals had no inflammatory changes in 4 weeks, however, in 8, 12 and 24 weeks in Balb/c. Wistar and C57BL/6 of the experimental group, mild to moderate chronic active gastritis was observed in antrum and body, which increased in severity over time, atrophy gastritis was still not seen in 24 weeks. In contrast, in the controls, no remarkable changes were detected. CONCLUSIONS: SS1 Hp can colonize in the glandular stomach mucosa of BALB/c, C57BL/6 mice and Wistar rats and leads to chronic active gastritis in long-term study. SS1 mouse and rat model is adaptable for animal experimentation of H. pylori including vaccine studies, screening for novel therapeutics and investigation of mechanisms of pathogenesis.

Animals↗

[Study on diagnostic value of analyzing argyrophilic nucleolar organizer regions in benign and malignant pleural effusions].

OBJECTIVE: To evaluate the diagnostic value of argyrophilic nucleolar organizer regions (AgNOR) measurement in benign and malignant pleural effusions. METHODS: Pleural effusions from 50 patients with proven malignant disease, 30 patients with benign disease were studied using the one-step silver staining method. Six cytologically atypical samples were also included in this study. RESULTS: The mean AgNOR count in malignant cells was significantly higher than that in benign mesothelial cells (7.6 +/- 1.4 vs 2.3 +/- 0.7, P < 0.01). The morphological features of AgNOR in malignant cells were mainly of diffuse type (80%), while in benign mesothelial cells, mainly of nucleolar type (90%). Among the six cytologically atypical samples, four were in the malignant range, two were in the benign limits, and these were proved by histopathology. CONCLUSION: AgNOR study may be useful in differential diagnosis of benign and malignant pleural effusions.

Diagnosis, Differential↗

[Effect of electroacupuncture on succinate dehydrogenase of gentamycin induced ototoxic cochlear hair cells in guinea pigs].

OBJECTIVE: To observe the effect of electroacupuncture (EA) on succinate dehydrogenase (SDH) of gentamycin (GE) induced ototoxic cochlear hair cells. METHODS: Preyer's reflex normal guinea pigs were selected and divided randomly into three groups: GE group, EA group, control group. Brainstem auditory evoked potential (BAEP) and SDH in the cochlear hair cells were taken as indexes. In the animals of GE group GE was alone injected intramuscularly 80 mg.kg-1.d-1 for 20 days, while in the animals of EA group GE and additional EA was applied once a day on Tinggong (SI19), Yifeng(SJ17) and Shenshu (UB23) points. EA lasted for 15 minutes. RESULTS: In the GE group BAEP reaction threshold rose markedly, while that rose slightly in EA group. The difference was significant between two groups (P < 0.05). The change of SDH within cochlear hair cells and degree of hair cells injury in the EA group were lower than those in GE group. CONCLUSIONS: EA therapy could relieve GE ototoxicity, protect SDH in cochlear hair cells and might be a possible mechanism of action of EA.

Animals↗

Longitudinal cohort analysis of lethal prostate cancer progression in transgenic mice.

PURPOSE: Human prostate cancer is variably lethal, shows heterogeneous progression, and exhibits a spectrum of histopathology. Traditional rodent models of prostate cancer lack these characteristics. An alternative, autochthonous model of prostate cancer consists of transgenic mice which develop prostate cancer due to prostatic expression of SV40 T antigen. Lethal progression of such cancers in individual mice has not been previously characterized. Studies were undertaken to characterize the longitudinal progression of prostate cancers in these transgenic mice. METHODS: A prospective longitudinal cohort study was undertaken to characterize prostate cancer volume, progression, lethality, and histological heterogeneity in a transgenic mouse model of prostatic adenocarcinoma. Fifty-one transgenic mice were followed prospectively to determine the age at onset of palpable tumor and age at cancer-related death. Tumor volume was followed longitudinally by magnetic resonance imaging (MRI) in a subset of these mice and lethal cancers were evaluated by histopathology. RESULTS: Primary tumors became palpable at 10-38 weeks of age. Palpable tumors always preceded lethal progression. Cancer death followed 2-9 weeks later, and age at cancer death varied from 24 to 39 weeks of age. The histopathological changes were heterogeneous. Primary tumors were detectable by MRI before they became detectable by palpation. MRI showed that, analogous to human prostate cancers, volume of early stage primary tumors did not necessarily predict age at cancer death. CONCLUSION: Prostate cancer in transgenic mice mimics heterogeneic tumor progression in human prostate cancer, providing a uniquely relevant pre-clinical model. Tumor detection by MRI and palpation are valid surrogate measures of tumor progression in this model.

Animals↗

Isolation, characterization, and mapping of two human potassium channels.

Two novel human genes encoding putative potassium channels, kH1 and kH2, were identified from a human fetal brain cDNA library. Sequence analysis showed that kH1 and kH2 are homologous to rat IK8 and rat K13, respectively. The kH1 encodes a polypeptide of 495 amino acids, which shares 88% and 95% identity to IK8 at the nucleotide and amino acid level, respectively. The kH2 encodes a polypeptide of 515 amino acids with 86% and 92% identity to K13 at the nucleotide and amino acid level, respectively. Northern blot studies revealed that one mRNA species, approximately 5kb, of the kH1 was expressed abundantly in tissues examined, including the heart, skeletal muscle, and less abundant in the brain, liver, kidney, and pancreas. Interestingly, an alternative spliced form of 2.4 kb mRNA species of the kH1 was also found in the brain. Unlike kH1, 2.4 kb of kH2 was expressed predominantly in the brain, placenta, and the skeletal muscle where it shared a differently spliced form of the kH2 mRNA, approximately 2.0 kb. Fluorescence in situ hybridization localized kH1 to the human chromosome 2p25 and kH2 to the human chromosome 20q13.

Amino Acid Sequence↗

Improved stability and electrophoretic properties of preformed fluorescent cationic dye-DNA complexes in a taps-tetrapentylammonium buffer in agarose slab gels.

High-resolution capillary electrophoresis sizing of preformed complexes of bis-intercalating fluorescent dyes with double-stranded DNA has been demonstrated using hydroxyethylcellulose and 3-[tris-(hydroxymethyl) methylamino]-1-propanesulfonic acid-tetrapentylammonium (Taps-NPe+4) buffers (S. M. Clark and R. A. Mathies, Anal. Chem. 69, 1355-1363, 1997). Such capillary electrophoresis separations were unattainable in conventional buffers containing other cations such as Tris+, Na+, and NH+4. We report here the behavior of preformed double-stranded DNA-dye complexes on agarose slab gel electrophoresis in 40 mM Taps-NPe+4, 1 mM H2EDTA, pH 8.2. Upon electrophoresis in this buffer (a) complexes formed at DNA base pairs:dye ratios ranging from 100:1 to 5:1 show the same mobility; (b) the half-lives of DNA-dye complexes with monointercalators are two- to threefold longer than those in commonly used Tris buffers; (c) there is little dye transfer between labeled and unlabeled DNA molecules; and (d) precise two-color sizing of preformed restriction fragment-dye complexes with fluorescent bisintercalators is achieved.

Buffers↗

Glucocorticoid repression of gonadotropin-releasing hormone gene expression and secretion in morphologically distinct subpopulations of GT1-7 cells.

Two morphologically distinct subpopulations of GT1-7 cells have been characterized and examined for their responsiveness to glucocorticoids. Type I cells have a neuronal phenotype, extending many lengthy processes, and express neuronal, but not glial, markers. Type II cells show weaker or negative immunostaining for neuronal markers and exhibit fewer processes. The effect of glucocorticoids on gonadotropin-releasing hormone (GnRH) secretion and gene expression was compared in type I and type II GT1-7 cells. For secretion studies, cells were attached to Cytodex beads and perifused with control medium or medium containing dexamethasone (dex). The high level of GnRH secreted by type I cells was slightly enhanced in the presence of dex, whereas dex rapidly and profoundly decreased the already low level of GnRH secreted by type II cells. Immunocytochemistry for GnRH showed dark reaction product in the cell bodies and processes of type I cells and little or no immunoreactivity in type II cells. Both the endogenous mouse GnRH mRNA and the transcriptional activity of a mouse GnRH promoter luciferase reporter gene plasmid were suppressed to a greater extent in type II cells than in type I. In electrophoretic mobility shift assays, there was no difference between type I and type II nuclear extracts in the pattern of protein-DNA complexes formed on two previously identified negative glucocorticoid response elements located at -237 to -201 and -184 to -150 bp of the mouse promoter. Both cell types contained glucocorticoid receptors (GR) by Western blot analysis. Cytosols from type I or type II cells were incubated with [3H]dex to obtain GR binding parameters. Binding data were consistent with a one-site model for dex binding in each case. Small differences in Kd (1.7 nM, type I; 3.1 nM, type II) or Bmax (approximately 3600 sites/cell, type I; approximately 1800 sites/cell, type II) were not likely to account for the differential sensitivity to dex treatment. In conclusion, nuclear alterations in type II cells leading to greater transcriptional susceptibility to dex, coupled with low GnRH storage levels, may be reflected in exquisite sensitivity of GnRH secretion to glucocorticoid repression. This represents the first example of a steroid hormone acting directly on GnRH-producing cells to alter GnRH secretion.

Animals↗

Cloning, mapping, and tissue distribution of a human homologue of the mouse jerky gene product.

Inactivation of the jerky gene by insertion of a transgene into the mouse genome results in epileptic seizures in transgenic mice. This finding indicates that the jerky gene plays an important role in inducing epilepsy syndromes in mice. We report here our efforts in cloning, chromosomal mapping, and analysis of tissue distribution of a novel human gene, the HHMJG, a homologue to the mouse jerky gene product. We have successfully identified a full length cDNA clone encoding a novel human protein homologous to the mouse jerky gene product. The finding was based on the result of an analysis of EST (expressed sequence tag) sequences of a clone from a human tonsil cDNA library. A 4.0 kb mRNA species of the HHMJG is abundantly expressed in the majority of human tissues examined, including brain and skeletal muscle. However, in the testes, two mRNA species of the HHMJG, approximately 2.0 and 4.0 kb, are abundantly expressed. Sequence analysis of the HHMJG cDNA indicates that it encodes a putative protein of 51 kD, which shares significant sequence homology to not only the mouse jerky gene product but also some nuclear regulatory proteins, such as centromere binding protein-B. The predicted nuclear localization of the HHMJG product suggests that this protein may function as a nuclear regulatory protein. The result of human chromosomal mapping shows that the HHMJG is located on human chromosome 11q21. Our identification of the HHMJG cDNA provides a potential gene candidate to further investigate the biological significance and clinical implications of the HHMJG in human epilepsy.

Amino Acid Sequence↗

Crystal structure of mouse CD1: An MHC-like fold with a large hydrophobic binding groove.

CD1 represents a third lineage of antigen-presenting molecules that are distantly related to major histocompatibility complex (MHC) molecules in the immune system. The crystal structure of mouse CD1d1, corresponding to human CD1d, at 2.8 resolution shows that CD1 adopts an MHC fold that is more closely related to that of MHC class I than to that of MHC class II. The binding groove, although significantly narrower, is substantially larger because of increased depth and it has only two major pockets that are almost completely hydrophobic. The extreme hydrophobicity and shape of the binding site are consistent with observations that human CD1b and CD1c can present mycobacterial cell wall antigens, such as mycolic acid and lipoarabinomannans. However, mouse CD1d1 can present very hydrophobic peptides, but must do so in a very different way from MHC class Ia and class II molecules.

Animals↗

A novel endothelin receptor type-B-like gene enriched in the brain.

We report here our effort of cloning and characterization of a novel human gene, which encodes a putative human endothelin receptor type B like protein (hET(B)R-LP), from a human hippocampus tissue cDNA library. hET(B)R-LP consists of 614 amino acids with seven putative transmembrane domains. The deduced amino acid sequence of hET(B)R-LP is 52% similar and 26.7% identical to human endothelin type B receptor. A 4.0 kb mRNA of hET(B)R-LP is abundantly expressed in the human brain. The results of in situ hybridization and reverse transcriptase in situ gene amplification reveal tissue distribution and cellular localization of signals of hET(B)R-LP mRNA in the neuronal cells, particularly concentrated in Purkinje cells of the cerebellum, and neuronal cells of the hippocampus of human brain, including pyramidal cells of Ammon's horn and granule cells of the dentate gyrus. A 4.0 kb mRNA of hET(B)R-LP is also less abundantly expressed in the liver and the placenta. Expression of recombinant protein, hET(B)R-LP/HA, in cells of COS7 and HEK293 transfected with plasmid DNA, hET(B)R-LP/HA/pcDNA1/Amp, was confirmed by Northern blot analysis and by immunofluorescence staining of cells with anti-HA antibody. Specific binding of radiolabeled ET-1 and ET-3 to membrane preparations and to intact cells expressing recombinant protein of hET(B)R-LP/HA did not show any significant difference of binding properties between cells transfected with plasmid DNA, hET(B)R-LP/HA/pcDNA1/Amp, and cells untransfected, including both COS7 cells and HEK293 cells. The results of assays of measuring Ca++ mobilization and cAMP production in HEK293 cells indicate that ET-1, ET-3, bombesin and neuropeptide Y are unable to produce any kind of significant difference of Ca++ mobilization and cAMP production between HEK293 cells expressing recombinant protein and HEK293 cells untransfected or HEK293 cells transfected with vector DNA only (pcDNA1/Amp) in functional assays performed. Therefore, its ligand and physiological significance of hET(B)R-LP remains to be discovered.

Amino Acid Sequence↗

Cloning and characterization of a novel human DNase.

The therapeutic significance of recombinant human DNase I in treating the patients with cystic fibrosis has risen our interests in identifying other human DNase I-like enzymes to study their biological significance. Here we described our work of cloning and characterization of a novel gene, which encodes a human protein homologous to human DNase I. A full length cDNA clone of this gene consists of 1290 bp, encoding a polypeptide of 306 amino acids. The deduced amino acid sequence of this novel human DNase (nhDNase) is 45% identical to that of human DNase I. Among sixteen human tissues examined by Northern Blot, high level expression of nhDNase was found in human liver and spleen. Recombinant protein of nhDNase was produced in a Baculovirus expression system and purified by chromatography and reverse-phase HPLC. Purified recombinant nhDNase migrated as a single band of about 33 kD molecular weight analyzed by SDS-PAGE. The DNase activity of nhDNase was demonstrated by assay of hydrolysis of S.S.DNA. Its activity was dependent upon the presence of divalent metal irons, calcium and magnesium. However, unlike bovine pancreas DNase I, nhDNase was not inhibited by G-actin of bovine muscle, which indicates the physiological significance of this enzyme in clinical implication.

Actins↗

Identification of cytochrome P4503A as the major enzyme sub-family responsible for the metabolism of 22,23-dihydro-13-O-[(2-methoxyethoxy)methyl]-avermectin B1 aglycone by rat liver microsomes.

1. Metabolism of 22,23-dihydro-13-O-[(2-methoxyethoxy)methyl]-avermectin B1 aglycone (MEM-H2B1), a new avermectin, by rat liver microsomes has been studied. Metabolites identified were formed by demethylation of the methoxyethoxymethoxy (MEM) side chain, loss of the MEM side chain, partial cleavage and further oxidation of the MEM side chain, and oxidation of the aglycone after cleavage of the MEM side chain. 2. The specific cytochrome P450 isoforms involved in the metabolism of MEM-H2B1 were identified through immunoinhibition studies. Among several antibodies prepared against various cytochrome P450s, only anti-rat P4503A IgG inhibited MEM-H2B1 metabolism by liver microsomes from the untreated rat. Moreover, troleandomycin, a selective suicide inhibitor for enzymes of the cytochrome P4503A family, inhibited the total metabolism by > 80%. These results clearly indicate that cytochrome P4503A is primarily responsible for the metabolism of MEM-H2B1. 3. Secondary metabolism was evident in the metabolism of MEM-H2B1 by dexamethasone and phenobarbital induced liver microsomes, where different isoform(s) of cytochrome P4503A could be involved in these multiple step reactions.

Animals↗

[Effects of calcium channel blockers and calmodulin inhibitors on the secretion of endothelin-1 in cultured endothelial cells].

OBJECTIVE: The study is to investigate the effects of calcium channel blockers and calmodulin inhibitors on the secretion of endothelin-1 (ET-1) in cultured endothelial cells from human umbilical veins. RESULTS: Results showed that calcium channel blockers verapamil (5.5 x 10(-6) mol/L, 5.5 x 10(-5) mol/L), diltiazen (2.4 x 10(-4) mol/L) and calmodulin inhibitors chlorpromazine (3.1 x 10(-5) mol/L, 3.1 x 10(-4) mol/L), berbamine (1.6 x 10(-5) mol/L, 1.6 x 10(-4) mol/L) significantly decreased medium ET-1 levels in cultured endothelial cells. CONCLUSION: It was also indicated that extracellular calcium influx and calmodulin activity were necessary to the secretion of ET-1. In addition, nitroglycerine (2.2 x 10(-3) mol/L) remarkably reduced medium ET-1 levels in cultured endothelial cells, which suggested that nitric oxide might inhibit the secretion of ET-1.

Alkaloids↗