Biomedical subjects

H Y Wang

Publications and source records attributed to H Y Wang.

At least 37 records · Page 2Linked to original sources

PubMed2001

Lithium treatment inhibits protein kinase C translocation in rat brain cortex.

RATIONALE: Lithium, an effective psychotropic agent, affects membrane phospholipid metabolism, interferes with phosphoinositide signal transduction, and antagonizes the biological activity of calcium, all major factors of protein kinase C (PKC) activation. Consequently, lithium may interfere with cellular functions requiring PKC. Supporting this hypothesis, lithium was found to inhibit increased neurotransmitter release upon PKC activation and to prevent phorbol ester-mediated PKC translocation. OBJECTIVES: The present study was undertaken to determine whether the frontal cortex of rats treated with lithium exhibits altered PKC activity and translocation in response to phorbol ester, K+, or serotonin (5-HT) receptor stimulation and to determine whether specific PKC isozymes are disproportionately affected. METHODS: Rats were fed either a normal diet or one enriched with LiCl. In cerebrocortical slices or synaptosomes, cytosolic and membranous PKC activity and translocation in response to stimuli were determined after partial purification with anion exchange chromatography. RESULTS: In brain slices, lithium treatment inhibited phorbol 12-myristate, 13-acetate (PMA)-, 5-HT-, or K+-induced PKC translocation from cytosol to membrane without affecting basal membrane or cytosolic PKC activity. In synaptosomes, lithium also attenuated PMA- or K+-evoked translocation of PKC. Immunoblotting with isozyme-specific PKC antibodies revealed that chronic lithium treatment reduced basal cytosolic alphaPKC and deltaPKC but increased membrane-associated zetaPKC immunoreactivities. Stimulation with PMA, 5-HT or K+ elicited translocation of alpha, beta and gammaPKC isozymes and PMA induced translocation of delta and epsilonPKC isozymes. Stimulus-mediated translocation of PKC isozymes was attenuated in cortical tissue obtained from animals that received lithium for 6 weeks. In synaptosomes, PMA- or K+-induced PKC translocation was attenuated by in vitro lithium or chronic lithium treatment. Neither rubidium nor cesium affected PKC activities or PMA-induced translocation. Suppression of PMA-elicited translocation by lithium was partially antagonized by Ca2+. CONCLUSIONS: Lithium treatment reduces PKC translocation induced by either stimulation of a cell surface receptor or by direct enzyme stimulation with phorbol ester. This effect leads to reduced PKC-mediated phosphorylation of cellular proteins and may be responsible for the pharmacotherapeutic action of lithium.

Administration, Oral↗

PubMed2001

Genome-wide analyses on loss of heterozygosity in hepatocellular carcinoma in Southern China.

BACKGROUND/AIMS: To conduct a genome-wide analysis of loss of heterozygosity (LOH) and its clinical significance in hepatocellular carcinoma (HCC) in Southern China where high incidence of HCC was documented. METHODS: LOH of 382 microsatellite loci on all autosomes were detected with polymerase chain reaction-based microsatellite polymorphism analyses in 104 HCC tumor tissues. RESULTS: High frequency of LOH (>55.7%) was observed on chromosome 1p, 1q, 2q, 3p, 4q, 6q, 8p, 9p, 13q, 16q, and 17p. LOH rates on loci D4S2964 (4q21.21), D8S277 (8p23.1-pter) and D17S938 (17p13.1-p13.3) were significantly higher in cases with positive HBsAg than in those with negative HBsAg. Similarly, LOH on loci D1S214 (lp36.3), D1S2797 (1p34) and D3S3681 (3p11.2-p14.2) were more frequently detected in tumors with intrahepatic metastasis than in those without. CONCLUSIONS: Status of LOH in HCC in Southern China is similar to that reported previously in other countries and areas. However, we firstly identified high-frequency LOH on chromosome 3p in HCC. Furthermore, HBV infection, as well as tumor intrahepatic metastasis, may be correlated with allelic losses on certain chromosome regions.

Adolescent↗

PubMed2001

SC35 plays a role in T cell development and alternative splicing of CD45.

Molecular diversity via alternative splicing is important for cellular function and development. SR proteins are strong candidate regulators of alternative splicing because they can modulate splice site selection. However, endogenous substrates for SR proteins are largely unknown, and their roles as splicing regulators in vertebrate development are unclear. Here we report that Cre-mediated conditional deletion of the prototypical SR protein SC35 in the thymus causes a defect in T cell maturation. Deletion of SC35 alters alternative splicing of CD45, a receptor tyrosine phosphatase known to be regulated by differential splicing during thymocyte development and activation. This study establishes a model to address the function of SR proteins in physiological settings and reveals a critical role of SC35 in a T cell-specific regulated splicing pathway.

Alternative Splicing↗

PubMed2001

Study on fluorescent property of degrading products of piperacillin and its analytical application.

The fluorimetric property of the degrading products of piperacillin has been studied in detail. The studies on degrading pH, degrading time, detection alkalinity and other corresponding analytical parameters of acid degradation have been made. Then fluorometry of piperacillin was established by producing its stable fluorescent products. The detection limit for acid degradation analytical method is 2.34 ng/ml, the linear range is 7.80-4.0 x 10(2) ppb. The analytical sensitivity, precision and stability of degrading products of acid degradation are satisfactory, which has been used for the determination of the trace piperacillin in human serum and urine with satisfactory results.

Humans↗

PubMed2001

Functional studies of bradykinin receptors in Chinese hamster ovary cells stably expressing the human B2 bradykinin receptor.

Bradykinin B1 and B2 receptors, members of the G-protein coupled receptor superfamily, are involved in inflammation and pain. Chinese hamster ovary (CHO) cells stably expressing the human B2 bradykinin receptor (CHO-B2) were used to characterize the signal transduction pathways associated with this receptor and its regulation. The selective B2 antagonist [3H]NPC17731 but not the selective B1 antagonist [3,4-prolyl-3,4-(3)H(N)]-[des-Arg10,Leu9]kallidin ([3H]DALKD) bound to CHO-B2 cell membranes with a Kd of 0.77 nM and a Bmax of 1087 fmol/mg protein. [3H]NPC17731 binding was inhibited by bradykinin ligands in the order: NPC17731 > bradykinin > kallidin >> DALKD > [des-Arg10] kallidin (DAKD), consistent with the pharmacological profile of B2 bradykinin receptors. The B2 agonist bradykinin and the B1/B2 agonist kallidin, but not the B1 agonist DAKD, increased [35S]GTP gamma S binding to the CHO-B2 cell membranes. The B2 bradykinin receptors were co-immunoprecipitated with G alpha q/11. In response to bradykinin stimulation, coupling of the B2 receptors to G alpha q/11 was increased by 10-fold. Bradykinin and kallidin, but not DAKD, induced intracellular calcium release in CHO-B2 cells, which was blocked by NPC17731 but not by DALKD. These results demonstrate that B2 bradykinin receptors directly coupled to G alpha q/11 to regulate intracellular calcium release. CHO-B2 cell is a useful system that can be applied to study the effect of potential agents that may influence the B2 receptor function.

Animals↗

PubMed2001

Costimulation of resting B lymphocytes alters the IL-4-activated IRS2 signaling pathway in a STAT6 independent manner: implications for cell survival and proliferation.

IL-4 is an important B cell survival and growth factor. IL-4 induced the tyrosine phosphorylation of IRS2 in resting B lymphocytes and in LPS- or CD40L-activated blasts. Phosphorylated IRS2 coprecipitated with the p85 subunit of PI 3' kinase in both resting and activated cells. By contrast, association of phosphorylated IRS2 with GRB2 was not detected in resting B cells after IL-4 treatment although both proteins were expressed. However, IL-4 induced association of IRS2 with GRB2 in B cell blasts. The pattern of IL-4-induced recruitment of p85 and GRB2 to IRS2 observed in B cells derived from STAT6 null mice was identical to that observed for normal mice. While IL-4 alone does not induce activation of MEK, a MEK1 inhibitor suppressed the IL-4-induced proliferative response of LPS-activated B cell blasts. These results demonstrate that costimulation of splenic B cells alters IL-4-induced signal transduction independent of STAT6 leading to proliferation. Furthermore, proliferation induced by IL-4 in LPS-activated blasts is dependent upon the MAP kinase pathway.

Adaptor Proteins, Signal Transducing↗

PubMed2001

beta-Catenin expression in the transitional cell zone of pilomatricoma.

BACKGROUND: beta-Catenin, a participant in the Wnt pathway, has been shown to play an important role in the morphogenesis of hair follicles and the formation of hair follicle-related tumours, including pilomatricomas. It has been observed that at least 75% of human pilomatricomas possess activating mutations in beta-catenin. These findings suggested that beta-catenin plays an important role in the tumorigenesis of pilomatricomas. However, the pattern of beta-catenin expression in pilomatricoma tissues is still unclear. Objectives To examine the expression of beta-catenin in human pilomatricomas by immunohistochemical staining. METHODS: Twenty-six formalin-fixed and paraffin-embedded samples of pilomatricoma tissue were studied. RESULTS: Most transitional cells of pilomatricoma expressed beta-catenin strongly, but the basophilic cells and shadow cells did not. beta-Catenin showed a prominent membranous immunoreactivity and a small amount of condensed cytoplasmic staining, but there was definitely no evidence of nuclear positivity. CONCLUSIONS: These findings imply that beta-catenin is primarily involved in cell-cell adhesion rather than cellular proliferation during pilomatricoma pathogenesis, and suggest that if beta-catenin is involved in pilomatricoma tumorigenesis and tumour growth, it plays an indirect role.

Adolescent↗

PubMed2001

Evidence that neurones accumulating amyloid can undergo lysis to form amyloid plaques in Alzheimer's disease.

AIMS: Amyloid has recently been shown to accumulate intracellularly in the brains of patients with Alzheimer's disease (AD), yet amyloid plaques are generally thought to arise from gradual extracellular amyloid deposition. We have investigated the possibility of a link between these two apparently conflicting observations. METHODS AND RESULTS: Immunohistochemistry and digital image analysis was used to examine the detailed localization of beta-amyloid(42) (A beta 42), a major component of amyloid plaques, in the entorhinal cortex and hippocampus of AD brains. A beta 42 first selectively accumulates in the perikaryon of pyramidal cells as discrete, granules that appear to be cathepsin D-positive, suggesting that they may represent lysosomes or lysosome-derived structures. AD brain regions abundantly populated with pyramidal neurones exhibiting excessive A beta 42 accumulations also contained evidence of neuronal lysis. Lysis of these A beta 42-burdened neurones apparently resulted in a local, radial dispersion of their cytoplasmic contents, including A beta 42 and lysosomal enzymes, into the surrounding extracellular space. A nuclear remnant was found at the dense core of many amyloid plaques, strengthening the idea that each amyloid plaque represents the end product of a single neuronal cell lysis. The inverse relationship between the amyloid plaque density and pyramidal cell density in the AD brain regions also supports this possibility, as does the close correlation between plaque size and the size of local pyramidal cells. CONCLUSIONS: Our findings suggest that excessive intracellular accumulation of A beta 42-positive material in pyramidal cells can result in cell lysis, and that cell lysis is an important source of amyloid plaques and neuronal loss in AD brains.

Aged↗

PubMed2001

Stimulated D(1) dopamine receptors couple to multiple Galpha proteins in different brain regions.

Previous studies have revealed that activation of rat striatal D(1) dopamine receptors stimulates both adenylyl cyclase and phospholipase C via G(s) and G(q), respectively. The differential distribution of these systems in brain supports the existence of distinct receptor systems. The present communication extends the study by examining other brain regions: hippocampus, amygdala, and frontal cortex. In membrane preparations of these brain regions, selective stimulation of D(1) dopamine receptors increases the hydrolysis of phosphatidylinositol/phosphatidylinositol 4,5-biphosphate. In these brain regions, D(1) dopamine receptors couple differentially to multiple Galpha protein subunits. Antisera against Galpha(q) blocks dopamine-stimulated PIP(2) hydrolysis in hippocampal and in striatal membranes. The binding of [(35)S]GTPgammaS or [alpha-(32)P]GTP to Galpha(i) was enhanced in all brain regions. Dopamine also increased the binding of [(35)S]GTPgammaS or [alpha-(32)P]GTP to Galpha(q) in these brain regions: hippocampus = amygdala > frontal cortex. However, dopamine-stimulated binding of [(35)S]GTPgammaS to Galphas only in the frontal cortex and striatum. This differential coupling profile in the brain regions was not related to a differential regional distribution of the Galpha proteins. Dopamine induced increases in GTPgammaS binding to Galpha(s) and Galpha(q) was blocked by the D(1) antagonist SCH23390 but not by D(2) receptor antagonist l-sulpiride, suggesting that D(1) dopamine receptors couple to both Galpha(s) and Galpha(q) proteins. Co-immunoprecipitation of Galpha proteins with receptor-binding sites indicate that in the frontal cortex, D(1) dopamine-binding sites are associated with both Galpha(s) and Galpha(q) and, in hippocampus or amygdala, D(1) dopamine receptors couple solely to Galpha(q). The results indicate that in addition to the D(1)/G(s)/adenylyl cyclase system, brain D(1)-like dopamine receptor sites activate phospholipase C through Galpha(q) protein.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed2001

The role of nitric oxide on cigarette smoke-induced programmed cell death in the gastric mucosa.

BACKGROUND: This study was designed to investigate the effect of cigarette smoking on apoptosis in the gastric mucosa and the role of nitric oxide (NO) in the gas phase and extracts in the tar phase in this pathological process. METHODS: Male Sprague-Dawley rats and human gastric epithelial cell line AGS were used in the study. RESULTS: Cigarette smoking significantly increased apoptotic bodies in the rat gastric mucosa. However, neither filtered cigarette smoke, in which most of the substances in the tar phase were removed, nor oral administration of the two cigarette smoke extracts produced any effect on apoptosis. Interestingly, in this experiment pretreatment with a NO donor, the chloroform extract (CE) could significantly increase apoptosis. In in vitro study, only the CE induced DNA fragmentation, which could be elevated further by preincubation with a NO donor. The same extract also elevated inducible nitric oxide synthase (iNOS) activity. Inhibition of iNOS by N(G)-nitro-L-arginine methylester hydrochloride (L-NAME) partially abolished CE-induced apoptosis. CONCLUSIONS: These findings suggested that exogenous and endogenous NO had a synergistic effect with substances in the tar phase to induce programmed cell death in gastric epithelial cells both in vivo and in vitro.

Analysis of Variance↗

PubMed2001

Linkage of hypertension to chromosome 2q14-q23 in Chinese families.

OBJECTIVES: To identify chromosome regions containing hypertension susceptibility genes in Chinese. SUBJECTS AND METHODS: A three-stage study was carried out in Chinese siblings ascertained through outpatient clinics. In the first stage, 283 affected sib-pairs from 79 nuclear families were subjected to a genome-wide scan with 240 microsatellite marker loci. The second stage focused on chromosome 2 with additional markers resulting in an average distance of 5 cM and used an independent sample of 637 affected sib-pairs from 161 families. In the third stage, a fine-scale mapping study on the suggestive region was performed in an independent set of 777 affected sib-pairs from 106 families. Fourteen markers were used with an average distance less than 2 cM. Non-parametric linkage analyses (NPL), parametric linkage analyses and transmission-disequilibrium tests were used to assess evidence for linkage and association. RESULTS: Three markers (D2S168 at 27.06 cM, D2S151 at 152.04 cM and D2S142 at 161.26 cM) on chromosome 2 with suggestive linkage to hypertension susceptibility genes were identified in the genome-wide scan. In stage II, the suggestive region around D2S151 and D2S142 was replicated, while the linkage around D2S168 was not. In the stage III fine-scale mapping study, multipoint linkage analyses showed LOD scores greater than 2.0 throughout a region between 157.16 cM and 162.46 cM (all P < 0.001) with a maximum peak of 2.24 (P= 0.00067) at 160.52 cM. We also observed a NPL Z-score peak of 3.27 at 157.55 cM (P= 0.00086). CONCLUSIONS: The results of a suggestive region on chromosome 2q14-q23 (D2S112-D2S2370) were consistent between each of the three studies. Interestingly, this region overlaps a syntenic region that contains blood pressure quantitative trait loci identified in rat models of hypertension. These data suggest that the region near D2S142 and D2S151 deserves to be further screened for hypertension susceptibility genes.

China↗

PubMed2001

Selected contribution: effects of ischemia-reperfusion on vascular contractility and alpha(1)-adrenergic-receptor signaling in the rat tail artery.

To determine the effects of ischemia-reperfusion (I/R) on alpha(1)-adrenergic-receptor (alpha(1)-AR) functions, alpha(1)-AR-mediated contraction, inositol phosphate (IP) accumulation, and alpha(1)-AR-G protein coupling were examined in the tail arteries of anesthetized rats after 60 min of ischemia and 60 min of reperfusion. The contractile response to norepinephrine (NE) was significantly increased after I/R, whereas the contractile response to KCl remained unchanged. This was accompanied by a 69% increase in NE-stimulated IP accumulation. Furthermore, receptor-stimulated coupling of alpha(1a)-AR to G alpha(q/11) proteins was increased, whereas the coupling of alpha(1b)-AR or alpha(1d)-AR to their G proteins was not altered by I/R. These changes in vascular alpha(1)-AR function occurred without concurrent alteration in expression levels of membrane alpha(1)-AR subtypes or in the associated G proteins. These data demonstrate that I/R increases alpha(1a)-AR-G(q/11) protein coupling and alpha(1)-AR-stimulated IP accumulation in the tail artery. The alterations in alpha(1)-AR signaling are associated with and may underlie the enhanced contractile response of the tail artery to adrenergic stimulation after I/R.

Adenylyl Cyclases↗

PubMed2001

Epidemiologic and clinical survey of Behcet's disease in Korea: the first multicenter study.

The prevalence of Behcet's disease is the highest in the East Asian and the Mediterranean countries. Behcet's disease is also distributed in the Asian countries, but the nationwide survey has not been performed in Korea yet. The Korean Study Group for Behcet's Disease, founded in 1999, conducted a multicenter, retrospective survey on epidemiologic and clinical features of the patients with Behcet's disease from 20 hospitals around the nation from 1997 to 1999. Of 3,497 patients, 1,527 were classified into complete or incomplete type of Behcet's disease according to the revised Shimizu's classification. The sex ratio was 1:1.75 with the female predominance. Geographical distribution showed the highest frequency in Seoul (38.5%). Clinically, 98.8% had oral ulcers, 83.2% had genital ulcers, 84.3% had skin lesions and 50.9% had ocular lesions. As for the minor clinical manifestations, articular symptoms were the most frequent. The pathergy test showed positive in 15.4% of patients and revealed a higher positive rate in males (20.2%) than in females (12.7%). In conclusion, we performed the first multicenter study on Behcet's disease in Korea and revealed the female predominance, higher frequency of ocular lesions, and lower positivity of pathergy test in the patients.

Adolescent↗

PubMed2001

Expression of liver cancer associated gene HCCA3.

AIM: To study and clone a novel liver cancer related gene, and to explore the molecular basis of liver cancer genesis. METHODS: Using mRNA differential display polymerase chain reaction (DDPCR), we investigated the difference of mRNA in human hepatocellular carcinoma (HCC) and paired surrounding liver tissues, and got a gene probe. By screening a human placenta cDNA library and genomic homologous extend, we obtained a full-length cDNA named HCCA3. We analyzed the expression of this novel gene in 42 pairs of HCC and the surrounding liver tissues, and distribution in human normal tissues by means of Northern blot assay. RESULTS: A full-length cDNA of liver cancer associated gene HCCA3 has been submitted to the GeneBank nucleotide sequence databases (Accession No. AF276707). The positive expression rate of this gene was 78.6% (33/42) in HCC tissues, and the clinical pathological data showed that the HCCA3 was closely associated with the invasion of tumor capsule (P=0.023) and adjacant small metastasis satellite nodules lesions (P=0.041). The HCCA3 was widely distributed in the human normal tissues, which was intensively expressed in lungs, brain and colon tissues, while lowly expressed in the liver tissues. CONCLUSION: A novel full-length cDNA was cloned and differentiated, which was highly expressed in liver cancer tissues. The high expression was closely related to the tumor invasiveness and metastasis,that may be the late heredited change in HCC genesis.

Adult↗

PubMed2001

Surgical treatment for concomitant fractures of the femoral neck and diaphysis: a treatment protocol.

Concomitant ipsilateral femoral shaft and neck fractures are difficult to treat. The standard protocol in our hospital is plates for diaphyseal fractures and lag screws or dynamic hip screws (DHS) fixations for the femoral neck fractures. We treated 21 patients with these complex fractures between 1988 and 1998 with this protocol. All patients were injured from high-energy trauma. There were 15 males and 6 females with an average age of 44 years. The average follow-up period is 50 months. All except one patient united well. During the follow-up period, neither non-union of the femoral neck fracture nor osteonecrosis of the femoral head was noted. There was also no malunion. There were twenty good results and one poor functional result. We conclude that plate on the shaft and sliding hip screws or separate screws in the hip are a reliable method for concomitant ipsilateral femoral neck and shaft fractures.

Adult↗

PubMed2001

[The primary role of central region of HC-pro of potato Y potyvirus in synergism of plant viruses].

Five deleted mutants of HC-Pro gene of Chinese isolate of potato Y potyvirus (PVY-C) were obtained by PCR mutation, and their plant expression vectors were constructed. They were transformed into tobacco K326 (Nicotina tabacum cv. K326) mediated by Agrobacterium. PCR and Southern blot analysis revealed that PVY-C HC-Pro gene and its deleted mutants were integrated into tobacco genome, and Western blot analysis showed that they were all expressed in transgenic tobacco plants. Furthermore, infection test demonstrated that the central region of PVY-C HC-Pro can mediate synergism of PVY-C/cucumber mosaic cucumovirus (CMV) and PVY-C/potato X potexvirus (PVX), identifying that it is functional domain in synergism.

Blotting, Southern↗

PubMed2001

[Coding region cDNA sequence cloning of rat neuroglobin gene, its polymorphism feature and tissue expression profile analysis].

The coding region cDNA sequence of rat neuroglobin (NGB) was obtained by RT-PCR technique using a degeneracy PCR primer pair based on previously reported cDNA sequence of human and mouse NGB gene. Result demonstrated that the coding region cDNA sequence of rat NGB gene is 456 bp in length, which could encode a protein of 151 amino acids. The rat NGB gene is highly homology with mouse (96%) and human (88%) NGB gene. However, several polymorphism sites were also detected in the rat NGB coding region: 113 t/c [L38P], 133 a/g [N45D], 388 a/g[R130G], 417 t/c. The cDNA sequence of rat NGB gene has been registered in GenBank under the accession number AF333245. Moreover, highly expression level of rat NGB in brain, liver, kidney, heart and skeletal muscle was detected by using multiple tissue RT-PCR technique, indicating the functional importance of this novel gene.

Amino Acid Sequence↗

PubMed2001

Naloxone increases vascular responsiveness in chronic morphine treated rats and facilitates intracellular signaling in cultured vascular cells.

AIM: To probe the changes of vascular responsiveness and intracellular signaling during opiate withdrawal syndrome. METHODS: Morphine withdrawal syndrome in rats was precipitated by iv naloxone following daily injection of increasing dose of morphine for 2 weeks, the changes in mean arterial blood pressure (MBP) caused by acetylcholine (ACh) were recorded. Isolated mesenteric vascular beds were perfused with Kreb's solution containing different concentration of drugs. The cytoplasmic Ca2+ ([Ca2+]i) in Fura 2-loaded cultured bovine aortic endothelial cells (aec) and smooth muscle cells (smc) were assayed. The positive immunoreaction to the phosphorylated cyclic AMP responsive element-binding protein (phospho-CREB) in cultured smc was calculated. RESULTS: Naloxone 2 mg/kg iv following chronic morphine treatment precipitated severe opiate withdrawal signs in company with blunted hypotensive effect of Ach that was the same as chronic morphine treated rats before withdrawal. In the mesenteric vascular beds from chronic morphine treated rats, the EC50 of pressor effect of norepinephrine (NE) was decreased from (2.06 +/- 0.38) to (1.14 +/- 0.21) micromol/L (n = 8, P < 0.01) after the perfusion solution containing morphine 20 micromol/L was replaced by Kreb's containing naloxone 25 micromol/L. Furthermore, NE-induced perfusion pressure increases were completely prevented by Kreb's contained morphine 40 micromol/L. Morphine acutely applied to control smc produced some variable and naloxone-reversible [Ca2+]i changes, but naloxone did not. However, naloxone increased [Ca2+]i in two thirds of smc preincubated with morphine 0.1 or 0.5 mmol/L for 48 h from (97 +/- 20) to (167 +/- 29) nmol/L (n = 9, P < 0.01) and from (106 +/- 19) to (225 +/- 48) nmol/L (n = 10, P < 0.01), respectively, and it also increased the ratio of positive immunoreaction to phospho-CREB from (7.7 +/- 3.2) % to (19.6 +/- 4.7) % (n = 6, P < 0.01) in smc preincubated with morphine 0.5 mmol/L. In addition, naloxone decreased [Ca2+]i from (146 +/- 34) to (78 +/- 24) nmol/L in one third morphine-preincubated aec (n = 10, P < 0.01). CONCLUSION: That naloxone enhances vascular responsiveness to NE in chronic morphine treatment rats may be relevant to [Ca2+]i transient facilitation in company with cAMP-dependent phosphorylation enhancement.

Animals↗