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1.
Obstet Gynecol ; 95(2): 284-90, 2000 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-10674595

RESUMEN

OBJECTIVE: To evaluate the effect of 17beta-estradiol (E2) on the ability of human neutrophils to produce nitric oxide (NO) and its effects on platelet activation. METHODS: The expression of neuronal nitric oxide synthase (nNOS) protein and the formation of NO by 17beta-E2-incubated neutrophils from men were studied in vitro (ten male volunteers, no medical-surgical antecedents, aged 25-45 years). Platelet aggregometry and changes in cyclic guanosine monophospate (cGMP) levels were used to bioassay the functionality of NO released from neutrophils. RESULTS: Incubation of neutrophils derived from men with physiologic concentrations of 17beta-E2 (10(-10) to 10(-8) mol/L) enhanced the expression of nNOS protein. 17Beta-E2-incubated neutrophils also showed a significant increase in their ability to generate NO measured by the conversion of [3H]-L-arginine to [3H]-L-citrulline. Furthermore, 17beta-E2-incubated neutrophils showed a greater ability to prevent adenosine diphosphate (ADP)-induced platelet activation. Moreover, increased levels of cGMP were found in the coincubation of platelets with 17beta-E2-treated neutrophils. CONCLUSION: These results suggest that 17beta-E2 increases the ability of human neutrophils to produce NO and therefore may contribute to cardiovascular disease protection.


Asunto(s)
Estradiol/farmacología , Neutrófilos/efectos de los fármacos , Óxido Nítrico Sintasa/efectos de los fármacos , Óxido Nítrico/biosíntesis , Activación Plaquetaria/efectos de los fármacos , Adulto , Western Blotting , Enfermedades Cardiovasculares/prevención & control , GMP Cíclico/metabolismo , Humanos , Masculino , Persona de Mediana Edad , Neutrófilos/enzimología , Neutrófilos/metabolismo , Óxido Nítrico Sintasa/biosíntesis , Óxido Nítrico Sintasa de Tipo I , Valores de Referencia
2.
Biol Chem ; 378(1): 31-7, 1997 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-9049062

RESUMEN

Detergent-permeabilized EGFR-T17 fibroblasts, which overexpress the human epidermal growth factor (EGF) receptor, phosphorylate both poly-L-(glutamic acid, tyrosine) and exogenous calmodulin in an EGF-stimulated manner. Phosphorylation of calmodulin requires the presence of cationic polypeptides, such as poly-L-(lysine) or histones, which exert a biphasic effect toward calmodulin phosphorylation. Optimum cationic polypeptide/calmodulin molar ratios of 0.3 and 7 were determined for poly-L-(lysine) and histones, respectively. Maximum levels of calmodulin phosphorylation were attained in the absence of free calcium, and a strong inhibition of this process was observed at very low concentrations (Ki = 0.2 microM) of this cation. The incorporation of phosphate into calmodulin occurred predominantly on tyrosine residue(s) and was stimulated 34-fold by EGF.


Asunto(s)
Calmodulina/metabolismo , Receptores ErbB/metabolismo , Células 3T3 , Animales , Permeabilidad de la Membrana Celular , Receptores ErbB/genética , Expresión Génica , Humanos , Ratones , Fosforilación , Proteínas Tirosina Quinasas/metabolismo
3.
Biochem J ; 326 ( Pt 2): 369-76, 1997 Sep 01.
Artículo en Inglés | MEDLINE | ID: mdl-9291107

RESUMEN

Although it has been demonstrated that NO inhibits the proliferation of different cell types, the mechanisms of its anti-mitotic action are not well understood. In this work we have studied the possible interaction of NO with the epidermal growth factor receptor (EGFR), using transfected fibroblasts which overexpress the human EGFR. The NO donors S-nitroso-N-acetylpenicillamine (SNAP), 1,1-diethyl-2-hydroxy-2-nitrosohydrazine (DEA-NO) and N-{4-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]butyl}propane -1, 3-diamine (DETA-NO) inhibited DNA synthesis of fibroblasts growing in the presence of fetal calf serum, epidermal growth factor (EGF) or EGF plus insulin, as assessed by [methyl-3H]thymidine incorporation. Neither 8-bromo-cGMP nor the cGMP-phosphodiesterase inhibitor zaprinast mimicked this effect, suggesting that NO is unlikely to inhibit cell proliferation via a cGMP-dependent pathway. SNAP, DEA-NO and DETA-NO also inhibited the transphosphorylation of the EGFR and its tyrosine kinase activity toward the exogenous substrate poly-l-(Glu-Tyr), as measured in permeabilized cells using [gamma-32P]ATP as phosphate donor. In contrast, 3-[morpholinosydnonimine hydrochloride] (SIN-1), a peroxynitrite-forming compound, did not significantly inhibit either DNA synthesis or the EGFR tyrosine kinase activity. The inhibitory action of DEA-NO on the EGFR tyrosine kinase was prevented by haemoglobin, an NO scavenger, but not by superoxide dismutase, and was reversed by dithiothreitol. The binding of EGF to its receptor was unaffected by DEA-NO. The inhibitory action of DEA-NO on the EGF-dependent transphosphorylation of the receptor was also demonstrated in intact cells by immunoblot analysis using an anti-phosphotyrosine antibody. Taken together, these results suggest that NO, but not peroxynitrite, inhibits in a reversible manner the EGFR tyrosine kinase activity by S-nitrosylation of the receptor.


Asunto(s)
Receptores ErbB/antagonistas & inhibidores , Óxido Nítrico/farmacología , Proteínas Tirosina Quinasas/antagonistas & inhibidores , Proteínas Tirosina Quinasas/metabolismo , Células 3T3 , Animales , Sitios de Unión/efectos de los fármacos , GMP Cíclico/fisiología , ADN/antagonistas & inhibidores , ADN/biosíntesis , Activación Enzimática/efectos de los fármacos , Receptores ErbB/metabolismo , Humanos , Ratones , Óxido Nítrico/metabolismo , Fosforilación/efectos de los fármacos , Especificidad por Sustrato/efectos de los fármacos , Compuestos de Sulfhidrilo , Superóxidos
4.
Arch Esp Urol ; 53(1): 73-5, 2000.
Artículo en Español | MEDLINE | ID: mdl-10730429

RESUMEN

OBJECTIVE: To emphasize that urological symptoms and signs can be the presenting features of Crohn's disease. METHODS: A case of enterovesical fistula in a patient with Crohn's disease is described. The patient presented with hematuria and mild voiding symptoms, but there were no GI or other symptoms. The clinical aspects, diagnostic methods (ultrasound, cystoscopy, rectosigmoidoscopy) and treatment are discussed. RESULTS/CONCLUSIONS: Although Crohn's disease is rare, it should be considered when making the differential diagnosis in patients who present with voiding symptoms and hematuria.


Asunto(s)
Enfermedad de Crohn/complicaciones , Fístula Intestinal/etiología , Intestino Delgado , Fístula de la Vejiga Urinaria/etiología , Adulto , Humanos , Masculino
5.
Arch Esp Urol ; 51(3): 296-7, 1998 Apr.
Artículo en Español | MEDLINE | ID: mdl-9622925

RESUMEN

OBJECTIVE: To describe a case of acute abdomen arising from an underlying urological condition. METHODS/RESULTS: Herein we describe a patient with acute abdomen arising from a pyonephrotic kidney with fistulization to the peritoneal cavity. The clinical manifestations disappeared following nephrectomy by the anterior approach and drainage of the intraperitoneal cavity. CONCLUSION: Although infrequent, it should be taken into account that peritoneal abscess and/or pyonephrosis can cause acute abdomen when they fistulize to the peritoneal cavity.


Asunto(s)
Abdomen Agudo/etiología , Absceso/complicaciones , Cavidad Peritoneal , Pielonefritis/complicaciones , Fístula Urinaria/etiología , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Enfermedades Renales/complicaciones
6.
Arterioscler Thromb Vasc Biol ; 16(10): 1263-8, 1996 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-8857923

RESUMEN

Endothelial cell (EC)-released agents are active regulators of vascular smooth muscle cell (VSMC) functions. The first aim of the present work was to analyze the effect of ECs on interleukin-1 beta (IL-1 beta)-induced NO production by SMCs. Bovine aortic ECs (BAECs) and BVSMCs in culture were used for the study. IL-1 beta (0.03 U/L) stimulated nitrite production by BVSMCs. This increase was smaller in the presence of BAECs. This effect was accompanied by reduced expression of inducible NO synthase (iNOS) in BVSMCs coincubated with BAECs, as analyzed by Western blot analysis. The reduction in iNOS protein expression was partially reversed by a polyclonal antibody against transforming growth factor-beta (TGF-beta). Furthermore, we examined the cytotoxic effect of the NO released from BVSMCs on both BAECs and the BVSMCs themselves. Incubation of BAECs with IL-1 beta-prestimulated BVSMCs induced EC toxicity, which was partially inhibited by an inhibitor of NO synthesis, NG-nitro-L-arginine methyl ester, or an inhibitor of iNOS expression, dexamethasone. No cytotoxic effect of IL-1 beta on BVSMCs themselves was detected. ECs modulate iNOS expression in SMCs by mechanisms that include a TGF-beta-dependent pathway. The NO released from SMCs exerts cytotoxic effects on the adjacent endothelium without altering the viability of the SMCs.


Asunto(s)
Endotelio Vascular/metabolismo , Músculo Liso Vascular/metabolismo , Óxido Nítrico/biosíntesis , Factor de Crecimiento Transformador beta/metabolismo , Animales , Bovinos , Comunicación Celular , Muerte Celular/efectos de los fármacos , Células Cultivadas , Técnicas de Cocultivo , Interleucina-1/farmacología
7.
Arch Esp Urol ; 53(1): 75-7, 2000.
Artículo en Español | MEDLINE | ID: mdl-10730430

RESUMEN

OBJECTIVE: To report a case of giant diverticulum of the bladder associated with inguinal hernia. METHODS/RESULTS: An uncommon case of giant diverticulum associated with inguinal hernia is presented and the literature reviewed. The enormous size of the diverticulum and the associated lower urinary tract obstruction arising from hyperplasia of the prostate required resolution of both conditions. This was achieved by diverticulectomy with herniorrhaphy and TURP. CONCLUSIONS: Diverticula of the bladder are associated with lower urinary tract obstruction that are generally caused by a prostatic condition. Hernia with bladder diverticulum is uncommon. The symptoms are usually scanty and cannot be distinguished from the voiding symptoms arising from prostatic involvement. Apart form the clinical findings, US, cystography or IVP are useful for diagnosis. Treatment is usually by surgical correction of both the bladder diverticulum and voiding obstruction from prostatic hyperplasia.


Asunto(s)
Divertículo/complicaciones , Hernia Inguinal/complicaciones , Enfermedades de la Vejiga Urinaria/complicaciones , Anciano , Humanos , Masculino
8.
Arch Esp Urol ; 53(1): 77-9, 2000.
Artículo en Español | MEDLINE | ID: mdl-10730431

RESUMEN

OBJECTIVE: A case of balanopreputial abscess containing gas in a patient with adhesion of the glans penis to preputial mucosa is presented. METHODS: The clinical features, diagnostic methods (penile ultrasound) and treatment (debridement + step (staged?) circumcision) are described. RESULTS/CONCLUSIONS: Severe phimosis and balanopreputial adhesions can cause urological complications as shown in the case described. Ultrasound demonstrated the presence of abscess and gas.


Asunto(s)
Absceso , Enfermedades del Pene , Absceso/diagnóstico por imagen , Absceso/terapia , Adulto , Gases , Humanos , Masculino , Enfermedades del Pene/diagnóstico por imagen , Enfermedades del Pene/terapia , Ultrasonografía
9.
Am J Physiol ; 272(2 Pt 2): H760-8, 1997 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-9124436

RESUMEN

Nitric oxide (NO) is a growth inhibitor for diverse cellular types. In the present study, we have found that the inhibition of NO production in bovine endothelial cells by an L-arginine competitive antagonist induces DNA replication and promotes the transition from prereplicative to replicative phases of the endothelial cell cycle and an increase in c-myc and c-fos oncogene-encoded protein expression. The inhibition of NO generation had, however, a markedly different outcome depending on the state of confluence of the cells, i.e., proliferation was found in subconfluent cells, whereas apoptosis occurred in confluent cells. Moreover, Western blot analysis revealed differences in the constitutive NO synthase expression in proliferating compared with growth-arrested cells. In conclusion, these results disclose an alternative mechanism of endothelial cell apoptosis at the confluent state, which is related to NO inhibition. Moreover, the fact that the apoptotic phenomenon occurred in the presence of growth factors indicates the existence of apoptotic mechanisms that do not require growth factor deprivation.


Asunto(s)
Apoptosis/fisiología , Endotelio Vascular/citología , Endotelio Vascular/fisiología , Hormonas/fisiología , Óxido Nítrico/fisiología , Animales , Aorta/citología , Aorta/metabolismo , Aorta/fisiología , Bovinos , Ciclo Celular , División Celular/fisiología , Células Cultivadas , Fragmentación del ADN , Endotelio Vascular/metabolismo , Óxido Nítrico/biosíntesis , Óxido Nítrico Sintasa/metabolismo , Proteínas Proto-Oncogénicas c-fos/metabolismo , Proteínas Proto-Oncogénicas c-myc/metabolismo , Timidina/metabolismo
10.
Circulation ; 94(1): 83-7, 1996 Jul 01.
Artículo en Inglés | MEDLINE | ID: mdl-8964122

RESUMEN

BACKGROUND: In recent studies, it has been hypothesized that the protective anti-ischemic effects of aspirin outweigh the effects of inhibition of platelet thromboxane A2 synthesis. Recently, we have found that the antiaggregating effects of aspirin significantly affect nitric oxide (NO) generation by neutrophils. METHODS AND RESULTS: The present study used circulating neutrophils from myocardial ischemic rabbits to assess the effect of aspirin on the circulating neutrophil-derived NO production and, subsequently, on the modulation of platelet activation. Neutrophils were obtained after 60 minutes of coronary artery occlusion followed by 60 minutes of reperfusion. Sham-operated animals were used as controls. The results demonstrated that aspirin stimulated the production of NO by neutrophils obtained from both sham-operated rabbits and rabbits with myocardial ischemia. However, neutrophils isolated from animals with myocardial ischemia showed an enhanced ability to generate NO in the presence of aspirin. As a functional in vitro marker, we observed that neutrophils had a NO-dependent, platelet-antiactivating effect in the presence of aspirin. In the absence of aspirin, ischemic neutrophils did not modify platelet activation, even though they produced increased amounts of NO. An inhibitory role of superoxide anion on the neutrophil-related antiplatelet effect was suggested because superoxide dismutase induced significant platelet inhibition by myocardial ischemic neutrophils in the absence of aspirin. CONCLUSIONS: Our results show that myocardial ischemia/reperfusion stimulates production of NO by circulating neutrophils, an effect that was enhanced in the presence of aspirin. These results suggest a novel interpretation of the protective effect of aspirin on myocardial ischemia damage.


Asunto(s)
Aspirina/farmacología , Isquemia Miocárdica/metabolismo , Neutrófilos/metabolismo , Óxido Nítrico/biosíntesis , Animales , Masculino , Neutrófilos/fisiología , Óxido Nítrico/fisiología , Activación Plaquetaria/efectos de los fármacos , Agregación Plaquetaria/efectos de los fármacos , Conejos , Superóxidos/metabolismo
11.
Arch Esp Urol ; 51(3): 293-5, 1998 Apr.
Artículo en Español | MEDLINE | ID: mdl-9622924

RESUMEN

OBJECTIVE: To describe an additional case of malakoplakia of the prostate. The etiopathogenesis, the histological and clinical features of this disease are analyzed and the literature briefly reviewed. METHODS/RESULTS: The pathological features of malakoplakia of the prostate in an elderly man with severe prostatic syndrome and recurrent urinary infections from E. Coli are described. The clinical manifestations disappeared following adenomectomy according to the Millin technique. CONCLUSION: Diagnosis of malakoplakia of the prostate is based on the pathological findings. The importance of the pathologist's role in the diagnosis of this condition, which will determine the treatment to follow, is therefore underscored.


Asunto(s)
Malacoplasia/diagnóstico , Enfermedades de la Próstata/diagnóstico , Humanos , Masculino , Persona de Mediana Edad
12.
Arch Esp Urol ; 51(3): 298-300, 1998 Apr.
Artículo en Español | MEDLINE | ID: mdl-9622926

RESUMEN

OBJECTIVE: To describe a case of erectile dysfunction as a result of traction on the fracture table. METHODS: We report on a 39-year-old man who developed erctile dysfunction postoperatively and for several months thereafter, following intramedullary nailing with the Grosse-Kept bolt type fixation system. RESULTS: The patient spontaneously recovered erectile function six months after orthopaedic treatment. CONCLUSION: Erectile dysfunction induced by orthopaedic fracture table is a complication that should be taken into account. There are many procedures available to reduce the risk of this complication.


Asunto(s)
Disfunción Eréctil/etiología , Fracturas del Fémur/terapia , Enfermedades del Sistema Nervioso/complicaciones , Conducción Nerviosa , Pene/inervación , Pene/fisiopatología , Tracción/efectos adversos , Adulto , Humanos , Masculino , Enfermedades del Sistema Nervioso/etiología , Enfermedades del Sistema Nervioso/fisiopatología
13.
Arch Esp Urol ; 51(4): 374-5, 1998 May.
Artículo en Español | MEDLINE | ID: mdl-9656559

RESUMEN

OBJECTIVE: The purpose of this paper is to emphasize that despite the undeniable advantages of urological instrumentation (insertion of a ureteral catheter, double-J catheter; percutaneous nephrostomy, etc.), it also carries some risks and complications. METHODS: We report three cases of iatrogenic urological complications due to use of endoscopic and percutaneous material. RESULTS/CONCLUSION: Urologists, and particularly the residents, are reminded that iatrogenic complications may occur even in the easiest and routine procedures of the medical activity.


Asunto(s)
Enfermedad Iatrogénica , Cateterismo Urinario/efectos adversos , Cateterismo Urinario/instrumentación , Enfermedades Urológicas/etiología , Humanos , Enfermedades Urológicas/epidemiología
14.
Circ Res ; 83(3): 279-86, 1998 Aug 10.
Artículo en Inglés | MEDLINE | ID: mdl-9710120

RESUMEN

Two NO synthase (NOS) isoforms have been described in vessels, an endothelial constitutive NOS (eNOS) and an inducible NOS (iNOS). The purpose of the present study was to examine the endothelium-dependent and endothelium-independent hypotensive response in aging rats, analyzing the ability of their vessels to produce NO. The studies were performed in 2 groups of euvolemic, conscious, male Wistar rats: aging rats (n=20, 18 months old) and young rats (n=20, 5 months old). The hypotensive responses to acetylcholine, bradykinin, and sodium nitroprusside were determined. Furthermore, the expression of the NOS isoforms by Western blot and the eNOS and iNOS activities, defined as Ca2+-dependent and Ca2+-independent conversion of [14C]L-arginine into [14C]L-citrulline, respectively, were also determined. In the aging rats, we found an impaired hypotensive response to acetylcholine and bradykinin (2 NO- and endothelium-dependent hypotensive agents) that was accompanied by a preserved hypotensive response to sodium nitroprusside. Aging rats also demonstrated an enhanced sensitivity response to the pressor effect of the L-arginine antagonist L-Nomega-nitro-L-arginine and a reduced vasoconstrictor response to angiotensin II. The inhibition of NO synthesis normalized the pressor effect of angiotensin II in the aging animals. Nitrite plus nitrate plasma levels were increased in aging rats. Furthermore, cGMP content was also higher in the aging vessels. In the aging aortas, the expression of both eNOS and iNOS isoforms was enhanced. However, in aging rats, the activity of the eNOS isoform was markedly reduced, a finding that was accompanied by the presence of iNOS activity. The vessel wall of aging rats showed an enhanced expression of eNOS and iNOS isoforms. However, eNOS activity was reduced in the aging animals. These findings could explain the impaired endothelium-dependent hypotensive response associated with aging.


Asunto(s)
Envejecimiento/metabolismo , Endotelio Vascular/enzimología , Óxido Nítrico Sintasa/biosíntesis , Acetilcolina/farmacología , Animales , Aorta/metabolismo , Arginina/análogos & derivados , Arginina/farmacología , Presión Sanguínea/efectos de los fármacos , Bradiquinina/farmacología , Calcio/metabolismo , Bovinos , Endotelio Vascular/efectos de los fármacos , Inducción Enzimática , Inhibidores Enzimáticos/farmacología , Masculino , Óxido Nítrico Sintasa/genética , Óxido Nítrico Sintasa de Tipo II , Óxido Nítrico Sintasa de Tipo III , Nitroprusiato/farmacología , Penicilamina/análogos & derivados , Penicilamina/farmacología , Ratas , Ratas Wistar , S-Nitroso-N-Acetilpenicilamina , Vasodilatadores/farmacología
15.
Am J Physiol ; 277(4): H1317-25, 1999 10.
Artículo en Inglés | MEDLINE | ID: mdl-10516166

RESUMEN

Despite the evidence that cytokines stimulate nitric oxide (NO) production by inducible nitric oxide synthase (iNOS), several reports recently demonstrated that the hypotensive response related to endothelial nitric oxide synthase (eNOS) activity could be inhibited by the same cytokines. The aim of the present work was to analyze whether NO generated by vascular smooth muscle cells (VSMC) could modify eNOS protein expression in endothelial cells. Bovine aortic endothelial cells (BAEC) and bovine VSMC (BVSMC) in coculture were used for the study. Interleukin-1beta (IL-1beta, 10 ng/ml)-treated BVSMC, which expressed iNOS protein, decreased eNOS protein expression in BAEC. The presence of NO antagonists N(omega)-nitro-L-arginine methyl ester (10(-3) mol/l) or N(G)-monomethyl-L-arginine (10(-3) mol/l) prevented the decrease in eNOS protein expression induced by IL-1beta-treated BVSMC. Surprisingly, two different NO donors, 3-morpholinosydnonimine (10(-4) mol/l) and S-nitroso-N-acetyl-D,L-penicillamine (10(-4) mol/l), failed to modify eNOS expression in BAEC, suggesting the existence of a diffusible mediator released from IL-1beta-treated BVSMC that acts on endothelial cells by reducing eNOS expression. The presence of NO antagonists reduced tumor necrosis factor-alpha (TNF-alpha) production by IL-1beta-stimulated BVSMC. This effect was also produced in the presence of a protein kinase G inhibitor, guanosine-5'-O-(2-thiodiphosphate) trilithium salt. A polyclonal antibody against TNF-alpha prevented eNOS expression in the BAEC-BVSMC coculture. In conclusion, NO by itself failed to modify eNOS protein expression in endothelial cells but increased TNF-alpha generation by IL-1beta-stimulated BVSMC and, in this way, reduced eNOS expression in the endothelium.


Asunto(s)
Endotelio Vascular/enzimología , Músculo Liso Vascular/metabolismo , Óxido Nítrico Sintasa/metabolismo , Óxido Nítrico/fisiología , Factor de Necrosis Tumoral alfa/fisiología , Animales , Aorta/citología , Aorta/enzimología , Aorta/metabolismo , Bovinos , Técnicas de Cocultivo , Endotelio Vascular/citología , Interleucina-1/farmacología , Músculo Liso Vascular/citología , Óxido Nítrico Sintasa de Tipo III
16.
Eur J Clin Invest ; 29(2): 93-9, 1999 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-10092995

RESUMEN

BACKGROUND: Inflammatory related cardiovascular disease, i.e. cardiac allograft rejection, myocarditis, septic shock, are accompanied by cytokine production, which stimulates the expression of inducible nitric oxide (iNOS). MATERIALS AND METHODS: The aim of the present study was to examine whether anti-inflammatory doses of acetylsalicylic acid (aspirin) could regulate iNOS protein expression in bovine vascular smooth muscle cells (BVSMCs) in culture. RESULTS: Interleukin 1 beta (IL-1 beta, 0.03 U mL-1) induced nitric oxide release by BVSMCs. Aspirin inhibited nitric oxide release from IL-1 beta-stimulated BVSMCs in a dose-dependent manner. In addition, aspirin significantly inhibited iNOS protein expression in BVSMCs and reduced the translocation of the nuclear factor-kappa B (NF-kappa B). Furthermore, aspirin and the blockade of NO generation by BVSMCs reduced the production of tumour necrosis factor alpha (TNF-alpha) by these cells. CONCLUSION: High doses of aspirin inhibited iNOS protein expression in BVSMCs and decreased NF-kappa B mobilization. The inhibition of iNOS expression by aspirin was further associated with a reduced ability of BVSMCs to produce TNF-alpha. This study could provide new mechanisms of action for aspirin in the treatment of the inflammation-related cardiovascular diseases.


Asunto(s)
Antiinflamatorios no Esteroideos/farmacología , Aspirina/farmacología , Músculo Liso/efectos de los fármacos , Óxido Nítrico Sintasa/metabolismo , Óxido Nítrico/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , 6-Cetoprostaglandina F1 alfa/metabolismo , Animales , Western Blotting , Enfermedades Cardiovasculares/tratamiento farmacológico , Bovinos , Células Cultivadas , Proteínas de Unión al ADN/análisis , Epoprostenol/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Interleucina-1/farmacología , FN-kappa B/metabolismo , Óxido Nítrico Sintasa de Tipo II
17.
Circ Res ; 85(11): 1020-6, 1999 Nov 26.
Artículo en Inglés | MEDLINE | ID: mdl-10571532

RESUMEN

Recent studies have postulated the contribution of nitric oxide (NO) released by the endothelium to the beneficial effects of estrogen. Despite a neuronal-type NO synthase (nNOS) described in neutrophils, less is known about the effect of estrogen in these cells. The aim of the present study was to analyze the expression of nNOS protein in human neutrophils under different estrogenic conditions. We first analyzed nNOS expression in neutrophils obtained from premenopausal women. During the first 2 days of the follicular phase (low circulating estrogen concentrations), nNOS expression in neutrophils was reduced with respect to that found in neutrophils obtained from the same donors during the ovulatory phase (high circulating estrogen concentrations). Moreover, the expression of nNOS protein in neutrophils obtained from postmenopausal women after transdermal estrogen therapy was markedly enhanced with respect to that observed before the treatment. In vitro incubation of neutrophils derived from men for 6 hours with 17beta-estradiol (10(-10) to 10(-8) mol/L) upregulated the expression of nNOS protein. The 17beta-estradiol receptor antagonists, tamoxifen (10(-8) mol/L) and ICI 182780 (10(-8) mol/L), inhibited the upregulation of nNOS protein induced by 17beta-estradiol. The putative functional implication was denoted by a reduced expression of the CD18 antigen on the surface of 17beta-estradiol-incubated neutrophils, which was accompanied by a decreased adhesive capacity. Both effects were prevented by an NO antagonist. In conclusion, the in vivo levels of circulating estrogen concentrations seem to be associated with the level of nNOS protein expression in neutrophils from women. Moreover, low doses of 17beta-estradiol upregulate nNOS protein expression in neutrophils from men. The increased ability of 17beta-estradiol-incubated neutrophils derived from men to produce NO reduced their adhesive properties.


Asunto(s)
Estradiol/farmacología , Terapia de Reemplazo de Hormonas , Ciclo Menstrual/fisiología , Neutrófilos/efectos de los fármacos , Óxido Nítrico Sintasa/biosíntesis , Óxido Nítrico/biosíntesis , Caracteres Sexuales , Adulto , Anciano , Antígenos CD18/metabolismo , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/metabolismo , Enfermedades Cardiovasculares/prevención & control , Adhesión Celular/efectos de los fármacos , Inducción Enzimática/efectos de los fármacos , Estradiol/análogos & derivados , Antagonistas de Estrógenos/farmacología , Femenino , Fulvestrant , Humanos , Hormona Luteinizante/sangre , Masculino , Persona de Mediana Edad , Neutrófilos/enzimología , Óxido Nítrico Sintasa/genética , Óxido Nítrico Sintasa de Tipo I , Posmenopausia , Premenopausia , Receptores de Estrógenos/efectos de los fármacos , Tamoxifeno/farmacología , omega-N-Metilarginina/farmacología
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