Biomedical subjects

W Bai

Publications and source records attributed to W Bai.

At least 19 recordsLinked to original sources

PubMed2006

Conversion of operating theatre from positive to negative pressure environment.

The severe acute respiratory syndrome (SARS) crisis led to the construction of a negative pressure operating theatre at a hospital in Hong Kong. It is currently used for treatment of suspected or confirmed airborne infection cases, and was built in anticipation of a return of SARS, an outbreak of avian influenza or other respiratory epidemics. This article describes the physical conversion of a standard positive pressure operating theatre into a negative pressure environment, problems encountered, airflow design, and evaluation of performance. Since entering regular service, routine measurements and observations have indicated that the airflow performance has been satisfactory. This has also been confirmed by regular air sampling checks. Computational fluid dynamics, a computer modelling technique, was used to compare the distribution of room air before and after the design changes from positive to negative pressure. The simulation results show that the physical environment and the dispersion pattern of bacteria in the negative pressure theatre were as good as, if not better than, those in the original positive pressure design.

Aerosols↗

PubMed2001

Antagonism between PTEN/MMAC1/TEP-1 and androgen receptor in growth and apoptosis of prostatic cancer cells.

PTEN/MMAC1/TEP-1 (PTEN) tumor suppressor and androgen receptor play important roles in prostatic tumorigenesis by exerting opposite effects on homeostasis of prostatic epithelium. Here, we describe a mutual repression and selective dominance between PTEN and the androgen receptor (AR) in the growth and the apoptosis of prostatic cancer cells. On the one hand, PTEN and an inhibitor of phosphoinositide 3-kinase repressed the transcriptional activity of the AR as well as androgen-induced cell proliferation and production of prostate-specific antigen. On the other hand, androgens protected prostate cancer cells from PTEN-induced apoptosis in an AR-dependent manner. Whereas the repression of the transcriptional activity of the AR by PTEN is likely to involve the down-regulation of AKT, androgens protected prostate cancer cells from PTEN-induced apoptosis without an effect on AKT activity, demonstrating a differential involvement of AKT in the interaction between PTEN and the AR. Our data suggest that the loss of PTEN function may induce tumorigenesis through unopposed activity of the AR as well as contribute to the resistance of prostate cancers to androgen ablation therapy.

Androgen Receptor Antagonists↗

PubMed2000

Molecular mechanisms of tumor necrosis factor alpha gene expression in monocytic cells via hyperglycemia-induced oxidant stress-dependent and -independent pathways.

Increased oxidative stress has been reported in vivo in the diabetic state via the production of reactive oxygen species (ROS). Such stress is bound to play a key role on activation of circulating monocytes, leading to the accelerated atherosclerosis observed in diabetics. However the exact molecular mechanisms of monocyte activation by high glucose is currently unclear. Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). TNFalpha accumulation in the conditioned media was increased 10-fold and mRNA levels were increased 11.5-fold by CHG. The following observations supported that both NF-kappaB and AP-1 mediated enhanced TNFalpha transcription by CHG: 1) A 295-base pair fragment of the proximal TNFalpha promoter containing NF-kappaB and AP-1 sites reproduced the effects of CHG on TNFalpha transcription in a luciferase reporter assay, 2) mutational analyses of both NF-kappaB and the AP-1 sites abrogated 90% of the luciferase activity, 3) gel-shift analysis using the binding sites showed activation of NF-kappaB and AP-1 in CHG nuclear extracts, and 4) Western blot analyses demonstrated elevated nuclear levels of p65 and p50 and decreased cytosolic levels of IkappaBalpha in CHG-treated monocytes. That ROS acted as a key intermediate in the CHG pathway was supported by the following evidence: 1) increased superoxide levels similar to those observed with PMA or TNFalpha, 2) increased phosphorylation of stress-responsive mitogen-activated protein kinases p38 and JNK-1, 3) counteraction of the effects of CHG on TNFalpha production, the 295TNFluc reporter activity, activation of NF-kappaB, and repression of IkappaBalpha by antioxidants and p38 mitogen-activated protein kinase inhibitors. The study suggests that ROS function as key components in the regulatory pathway progressing from elevated glucose to monocyte activation.

Acetylcysteine↗

PubMed2000

BLC expression in pancreatic islets causes B cell recruitment and lymphotoxin-dependent lymphoid neogenesis.

CXCR5, the receptor for B lymphocyte chemoattractant (BLC), is required for normal development of Peyer's patches, inguinal lymph nodes, and splenic follicles. To test the in vivo activity of BLC in isolation of other lymphoid organizers, transgenic mice were generated expressing BLC in the pancreatic islets. In addition to attracting B cells, BLC expression led to development of lymph node-like structures that contained B and T cell zones, high endothelial venules, stromal cells, and the chemokine SLC. Development of these features was strongly dependent on B lymphocytes and on lymphotoxin alpha1beta2 and could be reversed by blocking lymphotoxin alpha1beta2. These findings establish that BLC is sufficient to activate a pathway of events leading to formation of organized lymphoid tissue.

Animals↗

PubMed2000

MEKK1 activation of human estrogen receptor alpha and stimulation of the agonistic activity of 4-hydroxytamoxifen in endometrial and ovarian cancer cells.

Estrogens are mitogens that stimulate the growth of both normal and transformed epithelial cells of the female reproductive system. The effect of estrogens is mediated through the estrogen receptors, which are ligand-regulated transcription factors. Tamoxifen, a selective estrogen receptor modulator, functions as an estrogen receptor antagonist in breast but an agonist in uterus. In the current study, we show that coexpression of a constitutively active MEKK1, but not RAF or MEKK2, significantly increases the transcriptional activity of the receptor in endometrial and ovarian cancer cells. The expression of wild-type MEKK1 and an active Rac1, which functions upstream of MEKK1, also increased the activity of the receptor while coexpression of dominant negative MEKK1 blocked the Rac1 induction, indicating that endogenous MEKK1 is capable of activating the receptor. Additional experiments demonstrated that the MEKK1-induced activation was mediated through both Jun N-terminal kinases and p38/Hog1 and was independent of the known phosphorylation sites on the receptor. p38, but not Jun N-terminal kinases, efficiently phosphorylated the receptor in immunocomplex kinase assays, suggesting a differential involvement of the two kinases in the receptor activation. More importantly, the expression of the constitutively active MEKK1 increased the agonistic activity of 4-hydroxytamoxifen to a level comparable to that of 17beta-estradiol and fully blocked its antagonistic activity. These findings suggest that the uterine-specific agonistic activity of the tamoxifen compound may be determined by the status of kinases acting downstream of MEKK1.

Endometrial Neoplasms↗

PubMed2000

Effect of hormone replacement therapy on heart rate variability in postmenopausal women.

OBJECTIVE: To assess the characteristics of autonomic control of heart rate in postmenopausal women before and after hormone replacement therapy (HRT). METHODS: Time domain and spectral domain heart rate variability (HRV) were performed in 58 postmenopausal women before and after HRT. RESULTS: Compared with examinations at baseline, values of all HRV measurements in subjects given HRT were increased at the fourth month (P < 0.05), while they remained unchanged in the control group (P > 0.05). Results showed an inverse correlation between all measures of HRV and mean R-R interval in the treatment group. CONCLUSION: HRT reduces sympathetic drive in postmenopausal symptomatic women. HRV may be an index of imbalance of autonomic control in perimenopausal women.

Autonomic Nervous System↗

PubMed2000

[Evaluation on the compliance of livial therapy in peri and postmenopausal women].

OBJECTIVE: To evaluate the compliance of livial therapy in peri and postmenopausal women. METHODS: One hundred thirty four peri and postmenopausal women advised to take Livial were studied for persistency, efficacy and side effect of treatment. RESULTS: The mean age is 55.2 years old and post menopausal period is averaged 6.7 years. Their chief complaints were mainly climacteric symptoms(97.0%). Ninety percent of women took livial after prescription. 41.0% of women ceased the therapy after (0.7 +/- 0.8) years of treatment, while 26.2% of them restored after (0.3 +/- 0.2) years due to recurrence of symptoms. The major reason of cease was fear of cancer. The climacteric symptoms were well relieved while body mass index remained unchanged. The occurrence of vaginal bleeding, breast tenderness, edema and gastrointestinal symptoms was 5.6%, 19.7%, 8.2% and 9.0% respectively. The side effect was dose dependent. CONCLUSION: Postmenopausal women had well compliance to Livial despite of mild side effects and ceasing ratio.

Adult↗

PubMed2000

[A study of polysaccharide-protein complex and glycosyls in the tissue surrounding titanium implant of rabbit].

OBJECTIVE: The absorption of the polysaccharide-protein complex to the implant surface may be the first reaction between the implant and the surrounding tissue. So we observed the distribution and the relative amount of the polysaccharide-protein complex and glycosyls in order to find out the possible functions and changing rules of these substances. METHODS: 12 rabbits were selected according to the age, sex, weight, and health conditions. Bilateral mandibular premolar teeth of rabbits were extracted under abdomen anesthesia (2% glutababituratic acid), then 12 titanium implants were placed into the teeth extraction holes of one side and left the other side to be the control one. All of the implants were required to be placed 2 mm below the alveolar crest, and tissue closure was achieved with mattress and interrupted single sutures. Antibiotic injections were given to the rabbits in the following 3 days. The animals were sacrificed at the end of 1 week, 4 weeks and 24 weeks. Tissue blocks (4 mm x 4 mm x 4 mm) containing the titanium implants and the control ones were removed, then fixed with 10% formaldehyde for 2 weeks, and decalcified with 10% EDTA (pH7.0) for 8 weeks. Carefully removed the titanium implants, the tissue blocks were embedded into the paraffin wax, then the sections were obtained and stained using following methods. 1. Alcian Blue Method: Alcian blue (pH 2.5) staining displayed the acidic proteoglycans; Alcian blue (pH 1.0) displayed the proteoglycans containing sulfonyl; Alcian blue/periodix acid-shiff staining demonstrated the acidic and neutral proteoglycans respectively. Alcian blue-MgCl2 with different ionic concentration identified the different kinds of proteoglycans. 2. Lectin Method: 5 kinds of lectins were used to locate 5 kinds of glycosyls. 2.5 micrograms/ml ConA located the glucose; 10 micrograms/ml PNA located the galactose; 10 micrograms/ml WGA located the N-acetylglucosamine; 25 micrograms/ml PHA-E located N-acetylgalactosamine, 10 micrograms/ml WPL loacted the fucose. RESULTS: High level of proteoglycans and glycosyls were observed in the peri-implant connective tissue during all phases of the experiment. It was also observed that polysaccharide-protein complex and glycosyls reached a high level in new bone matrix as well as osteoblasts. CONCLUSION: Polysaccharide-protein complex and glycosyls do play an important role in the implant-bone attachment, and titanium compatibility and may be closely related to the bone metabolic activity.

Animals↗

PubMed1999

Evidence for an important role of serine 16 and its phosphorylation in the stabilization of c-Mos.

The c-Mos serine/threonine protein kinase is an essential component of cytostatic factor (CSF), which is required for metaphase II arrest of eggs in vertebrates. Previously, we showed that c-Mos residue Ser-16 is phosphorylated in the ts110 Mo-MuSV-encoded Gag-Mos fusion protein. Here we provide evidence that Mos is phosphorylated at Ser-16 in transfected COS-1 cells. To investigate the role of this phosphorylation, Ser-16 was substituted with alanine or glutamic acid in full-length v-Mos (an Env-Mos fusion protein that contains 31 additional amino acids at the amino terminus of c-Mos), its mouse c-Mos equivalent version (v-Mos residues 32-374, hereafter referred to as Mos), and mouse c-Mos. Constructs expressing mutant versions of Mos were transfected into COS-1 and NIH3T3 cells in a transient and stable manner, respectively. Synthesis and proteolysis of Mos were evaluated by pulse-chase analysis of 35S-methionine-labeled proteins. Our findings indicate that the S16A mutant of Mos was highly unstable. It accumulated to approximately 10% of the level of wild-type Mos or its S16E mutant. In addition, the S16A mutation but not the S16E mutation inhibited Mos interaction with a cellular protein, p35, suggesting that phosphorylation at Ser-16 may promote Mos interaction with p35. As expected from its destabilizing effect, the S16A mutation caused a dramatic decrease in the cellular transforming activity of Mos (determined by soft-agar colony-formation assay with the stably transfected NIH3T3 cells), which is known to correlate with its CSF function. Efficient ubiquitin-mediated proteolysis of c-Mos requires proline as the second residue from the amino-terminus. In contrast to Mos, neither the stability nor protein kinase activity of v-Mos (in which c-Mos residue Pro-2 becomes Pro-33) was affected by the S16A mutation. To provide further proof that, similar to c-Mos, the S16A mutant is recognized by the proteolysis system through Pro-2, we show that the effect of the S16A mutation is reversed by the Pro-2-Ala mutation. Thus, our results indicate that Ser-16 has an important role in the regulation of c-Mos and that phosphorylation at Ser-16 may inhibit proteolysis of c-Mos.

3T3 Cells↗

PubMed1999

Angiotensin II signaling in vascular smooth muscle cells under high glucose conditions.

The mechanisms responsible for the accelerated cardiovascular disease in diabetes, as well as the increased hypertrophic effects of angiotensin II (Ang II) under hyperglycemic conditions, are not very clear. We examined whether the culture of vascular smooth muscle cells (VSMC) under hyperglycemic conditions to simulate the diabetic state can lead to increased activation of key growth- and stress-related kinases, such as the mitogen-activated protein kinases (MAPKs), in the basal state and in response to Ang II. Treatment of porcine VSMC for short time periods (0.5 to 3 hours) with high glucose (HG; 25 mmol/L) markedly increased the activation of the extracellular signal-regulated kinase (ERK1/2) and c-Jun/N-terminal kinase (JNK) relative to cells cultured in normal glucose (NG; 5.5 mmol/L). p38 MAPK also was activated by HG, and this effect remained sustained for several hours. Ang II treatment increased the activity of all 3 families of MAPKs. Ang II-induced ERK activation was potentiated nearly 2-fold in cells treated with HG for 0.5 hour. However, Ang II-induced JNK was not altered. In VSMC cultured for 24 hours with HG, Ang II and HG displayed an additive response on p38 MAPK activity. MAPKs can lead to activation of transcription factors such as activator protein-1 (AP-1). HG alone significantly increased AP-1 DNA-binding activity. Furthermore, Ang II and HG combined had additive effects on AP-1 activity. These results suggest that increased activation of specific MAPKs and downstream transcription factors, such as AP-1, may be key mechanisms for the increased VSMC growth potential of HG alone and of Ang II under HG conditions.

Angiotensin II↗

PubMed1999

Hyperglycemia-induced activation of nuclear transcription factor kappaB in vascular smooth muscle cells.

The transcriptional nuclear factor (NF)-kappaB can be activated by diverse stimuli such as cytokines, mitogens, oxidative stress, and lipids, leading to the transactivation of several genes that play important roles in the development of atherosclerosis. Because oxidative stress may play a key role in the pathogenesis of diabetic vascular disease, we have examined whether culture of porcine vascular smooth muscle cells (PVSMCs) under high glucose (HG) conditions (25 mmol/l) to simulate the diabetic state can lead to the activation of NF-kappaB, and also whether cytokine- or growth factor-induced NF-kappaB activation is altered by HG culture. We observed that PVSMCs cultured in HG showed significantly greater activation of NF-kappaB in the basal state compared with cells cultured in normal glucose (NG) (5.5 mmol/l). Treatment of the cells with cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin-1beta, or with growth factors, such as platelet-derived growth factor, insulin-like growth factor-I, and epidermal growth factor, all led to NF-kappaB activation in cells cultured in both NG and HG. However, their effects were markedly greater in HG. The augmented TNF-alpha-induced NF-kappaB activation in HG was associated with increased TNF-alpha-mediated transcriptional activation of the vascular cell adhesion molecule-1 promoter. Immunoblotting with an antibody to the p65 subunit of NF-kappaB indicated that the levels of this protein were higher in the nuclear extracts from cells cultured in HG compared with NG. Cells cultured in HG also produced significantly greater amounts of the reactive oxygen species superoxide. HG-induced NF-kappaB activation was inhibited by a protein kinase C inhibitor, calphostin C. These results suggest that hyperglycemia-induced activation of NF-kappaB in VSMCs may be a key mechanism for the accelerated vascular disease observed in diabetes.

Animals↗

PubMed1999

[Effect of conjugated estrogen and Org OD14 on serum lipoprotein and apolipoprotein in perimenopausal and postmenopausal women].

OBJECTIVE: To determine the effect of conjugated estrogen and Org OD14 on serum lipoprotein and apolipoprotein in perimenopausal women. METHOD: 74 patients were divided into 2 groups: 46 were given conjugated estrogen 0.625 mg and medroxyprogesterone acetate 4 mg daily according to the continuous sequential, regimen 28 were given Org OD14 2.5 mg every two days. Serum lipoprotein and apolipoprotein estradiol and follicle stimulating hormone were measured before and (one and two years) after treatment. RESULTS: Total Cholesterol (TC), Triglycerin (TG), high density lipoprotein (HDL-C), Apolipoprotein AI (Apo AI), Apolipoprotein AII (Apo AII), Apolipoprotein B(Apo B), Apolipoprotein CII(Apo CII), Apolipoprotein CIII(Apo CIII), Lipoprotein(a)[Lp(a)] increased significantly (P < 0.05), while ApoB/AI, ApoCII/CIII decreased significantly(P < 0.05) in conjugated estrogen group. ApoCIII, E decreased, while ApoAI/AII increased significantly (P < 0.05) in Org OD14 group. After two years treatment, TC, HDL-C, ApoAI, ApoCIII, ApoE, TC, HDL-C, ApoAI, ApoCIII, ApoE of conjugated estrogen group were higher than those of Org OD14 group(P < 0.05), ApoCII/CIII of Conjugated estrogen was lower than that of Org OD14 group(P < 0.05). CONCLUSION: Postmenopausal hormone replacement therapy regulates the constitution of serum lipoprotein and apolipoprotein.

Adult↗

PubMed1999

[DNA polymorphism of Vibrio cholera and other vibrios].

OBJECTIVE: To investigate the inherent characteristics of V. cholera and other vibrios and the association between them. METHODS: Polymerase chain reaction (PCR), DNA sequences analysis, randomly amplified polymorphic DNA (RAPD) and average linkage cluster analysis were used to study V. cholera including 3 strains of O139, 4 strains of E1 Tor biotype, 3 strains of classical and 3 other vibrios. RESULTS: V. cholera O139 contained the genomic sequences of CTX A2-B as well as O1 V. cholera, indicating that their homologous nucleotides was 96.9%-98.7%, and other vibrios did not contain CTX. O1 V. cholera and other vibrios were divided into 4 groups by RAPD: classical; O139 and E1 Tor; V. paraheamolyticus and V. vulnificus; and V. flluvialis. The O139 DNA fingerprints of RAPD were almost as same as E1 Tor biotype, whose average linkage cluster distance was 0, similar with classical biotype, whose average linkage cluster distance was 2.07, much different from V. paraheamolyticus and others with the average linkage cluster distance being 6.76-8.54. CONCLUSION: V. cholera and other vibrios are polymorphic in inherent characteristics. Being as same as the inherent characteristics of E1 Tor, O139 may evoluted from E1 Tor biotype. And also the inherent characteristics of V. parahemolytisus were as same as those of V. vulnificus.

DNA, Bacterial↗

PubMed1998

The ovo gene required for cuticle formation and oogenesis in flies is involved in hair formation and spermatogenesis in mice.

The Drosophila svb/ovo gene gives rise to differentially expressed transcripts encoding a zinc finger protein. svb/ovo has two distinct genetic functions: shavenbaby (svb) is required for proper formation of extracellular projections that are produced by certain epidermal cells in late-stage differentiation; ovo is required for survival and differentiation of female germ cells. We cloned a mouse gene, movo1 encoding a nuclear transcription factor that is highly similar to its fly counterpart in its zinc-finger sequences. In mice, the gene is expressed in skin, where it localizes to the differentiating cells of epidermis and hair follicles, and in testes, where it is present in spermatocytes and spermatids. Using gene targeting, we show that movo1 is required for proper development of both hair and sperm. movo1(-/-) mice are small, produce aberrant hairs, and display hypogenitalism, with a reduced ability to reproduce. These mice also develop abnormalities in kidney, where movo1 is also expressed. Our findings reveal remarkable parallels between mice and flies in epidermal appendage formation and in germ-cell maturation. Furthermore, they uncover a phenotype similar to that of Bardet-Biedl syndrome, a human disorder that maps to the same locus as human ovo1.

Amino Acid Sequence↗

PubMed1998

[Complex surgical therapy for severe hepatic trauma].

OBJECTIVE: To improve the result of surgical therapy for patients with severe hepatic injury. METHODS: Retrospective analysis was made on the result of surgical treatment of 237 patients with hepatic trauma during the past 8 years. 180 patients underwent surgery. Procedures such as packing with the omentum for the laceration of hepatic parenchyma, debridement or irregular hepatectomy under the direct control of lacerated hepatic blood vessels or Pringle's maneuvre and selective ligation of hepatic artery were used for patients with severe hepatic injury (Grad III-V). RESULTS: Among the 180 patients, 154 were cured, and 8 of 23 with posthepatic IVC injury were cured with the maximum blood transfusion of 12,000 ml. The overall morality rate was 11.8%(28 of 237 patients). Besides associated injuries inside and outside the abdomen, exsanguination with or without coagulopathy was the main cause of death. CONCLUSION: Accurate liver packing with appropriate adjunctive procedures is effective in the treatment of retrohepatic venous injury.

Adolescent↗

PubMed1997

An interaction between DNA ligase I and proliferating cell nuclear antigen: implications for Okazaki fragment synthesis and joining.

Although three human genes encoding DNA ligases have been isolated, the molecular mechanisms by which these gene products specifically participate in different DNA transactions are not well understood. In this study, fractionation of a HeLa nuclear extract by DNA ligase I affinity chromatography resulted in the specific retention of a replication protein, proliferating cell nuclear antigen (PCNA), by the affinity resin. Subsequent experiments demonstrated that DNA ligase I and PCNA interact directly via the amino-terminal 118 aa of DNA ligase I, the same region of DNA ligase I that is required for localization of this enzyme at replication foci during S phase. PCNA, which forms a sliding clamp around duplex DNA, interacts with DNA pol delta and enables this enzyme to synthesize DNA processively. An interaction between DNA ligase I and PCNA that is topologically linked to DNA was detected. However, DNA ligase I inhibited PCNA-dependent DNA synthesis by DNA pol delta. These observations suggest that a ternary complex of DNA ligase I, PCNA and DNA pol delta does not form on a gapped DNA template. Consistent with this idea, the cell cycle inhibitor p21, which also interacts with PCNA and inhibits processive DNA synthesis by DNA pol delta, disrupts the DNA ligase I-PCNA complex. Thus, we propose that after Okazaki fragment DNA synthesis is completed by a PCNA-DNA pol delta complex, DNA pol delta is released, allowing DNA ligase I to bind to PCNA at the nick between adjacent Okazaki fragments and catalyze phosphodiester bond formation.

Chromatography, Affinity↗

PubMed1997

Differential phosphorylation of chicken progesterone receptor in hormone-dependent and ligand-independent activation.

Many steroid receptors, including chicken progesterone receptor, have been shown to be activated in the absence of their cognate ligands by modulators of kinases and phosphatases. To investigate the molecular mechanism of ligand-independent activation, chicken progesterone receptor mutants in which either one or all four of the previously identified phosphorylation sites have been changed to nonphosphorylatable alanine were analyzed for their ability to be activated by progesterone, 8-bromoadenosine 3':5'-cyclic monophosphate, or a dopamine agonist, SKF82958. Our current study shows that the receptor is differently phosphorylated in ligand-dependent and ligand-independent activation. The transcriptional activity of the receptor in response to 8-bromoadenosine 3':5'-cyclic monophosphate is affected by mutation of either Ser211 or Ser260. In addition, our data demonstrated that none of the four sites is absolutely required for the activation of the receptor by either 8-bromoadenosine 3':5'-cyclic monophosphate or the dopamine agonist. Treatment with 8-bromoadenosine 3':5'-cyclic monophosphate did not increase the overall level of receptor phosphorylation or cause phosphorylation of the receptor at alternate sites. These data raise the possibility that ligand-independent activation of the chicken progesterone receptor may be mediated through changes in the phosphorylation of coregulators or other protein factors interacting with the receptors.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1997

The role of nitric oxide in the regulation of aldosterone synthesis by adrenal glomerulosa cells.

The role of nitric oxide (NO) in the regulation of aldosterone synthesis in the adrenal glomerulosa is not known. In this study, we observed that liberators of NO such as S-nitroso-N-acetyl-penicillamine (SNAP), sodium nitroprusside (Snp) and spermine nonoate (SNO) could significantly inhibit angiotensin II (AII) and ACTH-induced aldosterone synthesis in isolated rat and cultured human adrenal glomerulosa cells. To evaluate more precisely whether glomerulosa cells express NO synthase, we performed immunoblotting experiments with antibodies specific for the endothelial type ecNO synthase as well as the neuronal NO synthase. This revealed the presence of the ecNO synthase in rat adrenal capsules, in normal and in adenomatous human adrenal glomerulosa tissue, as well as in freshly dispersed rat adrenal glomerulosa cells. Furthermore, on immunohistochemical analysis, rat adrenal glomerulosa cell sections showed strongly positive staining for ecNO synthase. These results suggest that NO may be an important negative modulator of adrenal glomerulosa steroidogenesis.

Adrenocorticotropic Hormone↗