Examinando por Materia "Endothelium"

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  • Publicación
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    Plasma nitrate levels and flow-mediated vasodilation in untreated
    (2011-05) García, Ronald G.; Zarruk, Juan G.; Barrera, Carlos; Pinzón, Alexander; Trillos, Elizabeth; Arenas, William D.; Luengas, Carlos; Tomaz, Carlos A.; Lopez-Jaramillo, Patricio
    Objective: Findings from several studies have revealed that major depression is associated with an increased cardiovascular risk. The physiopathologic mechanisms of this association remain unclear, although recently, it has been hypothesized that a decreased production of nitric oxide could be a potential contributor to vascular dysfunction in depressive patients. The objective of this study was to evaluate nitric oxide production and vascular endothelial function in treatment-naive young healthy adults with a first episode of major depression. Methods: A case-control study in 50 treatment-naive young adults with a first episode of major depression and 50 healthy control subjects was conducted. Plasma levels of nitric oxide metabolites (nitrates/nitrites) were determined using a colorimetric assay based on Griess reaction. Endothelial function was assessed by flow-mediated vasodilation measurements after reactive hyperemia. Results: The mean age of the depressed patients was 22.6 (standard deviation [SD], 4.6) years, whereas the controls were 23.4 (SD, 4.8) years. Sixteen men (32%) and 34 women (68%) were included in each group. The plasma nitrite/nitrate concentrations were significantly lower in depressive subjects compared with healthy controls (17.5 [SD, 4.9] Kmol/L versus 21.6 [SD, 7.0] Kmol/L, p G .001); however, flow-mediated vasodilation values were similar in both groups (13.1% [SD, 4.3%] versus 12.1% [SD, 5.0%], p = .10). Conclusions: Decreased plasma concentrations of nitric oxide metabolites are not associated with vascular endothelial dysfunction in young subjects with a first episode of major depression. Reduced nitrate/nitrite levels could reflect a decreased nitric oxide production in the central nervous system of depressed subjects. Further studies are needed to confirm this hypothesis.
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    The role of the L-arginine-nitric oxide pathway in preeclampsia
    (2008-08-01) Lopez-Jaramillo, Patricio; Arenas, William D.; García, Ronald G.; Rincón, Melvin Y.; López Casillas, Marcos
    : Preeclampsia (PE) is a major cause of maternal and perinatal mortality, especially in developing countries. Its etiology involves multiple factors, but no specific cause has been identified. Evidence suggests that clinical manifestations are caused by endothelial dysfunction. Nitric oxide (NO), which is synthesized from L-arginine in endothelial cells by the endothelial nitric oxide synthase (eNOS), provides a tonic dilator tone and regulates the adhesion of white blood cells and platelet aggregation. Alterations in the L-arginine-NO pathway have been associated with the development of PE. Various studies, reporting decreased, elevated or unchanged levels of nitrite (NO2) and nitrate (NO3), two end products of NO metabolism, have been published. Our group contributed to those contradictory reports describing cases of PE with both elevated and decreased levels of NO2 and NO3. Apparently, diminished levels of NO could be related to deficiencies in the ingestion of dietary calcium associated to low levels of plasma ionic calcium, which is crucial to the eNOS’ activity. Also, low levels of NO could be associated with the presence of eNOS polymorphisms or the presence of increased levels of ADMA, the endogenous inhibitor of NO. High levels of NO associated to low levels of cGMP suggest a decreased bioactivity of NO, which is probably related to an increased degradation of NO caused by a high production of superoxide in states of infection and inflammation. The present article analyses and reviews the reported paradoxical roles of the L-arginine-NO pathway in PE and gives a possible explanation for these results.
  • Publicación
    Acceso abierto
    Subclinical infection as a cause of inflammation in preeclampsia
    (2008-07) Lopez-Jaramillo, Patricio; Casas Herrera, Julián Augusto; Arenas Mantilla, Mario; Jáuregui, Isabel E.; Mendoza, Mayaris A.
    Preeclampsia, a pregnancy-exclusive hypertensive disorder, is the major cause of maternal and perinatal mortality, with a greater importance in developing countries. The role of inflammation in the pathogenesis of preeclampsia has been the object of recent studies by our group. We have described elevated levels of inflammatory markers (tumor necrosis factor alpha, interleukin-6, and C-reactive protein) in preeclamptic patients and demonstrated that Latin-American women present a higher degree of inflammation than women from developed countries. We have results that suggest that chronic subclinical infections and insulin resistance are the most probable causes of the increased inflammation in preeclampsia. Moreover, we showed that early treatment of urinary and vaginal infections decreased the incidence of preeclampsia. We also have evidence that suggests that inflammation leads to endothelial dysfunction, predisposing women to develop preeclampsia. Increased levels of inflammation markers and endothelial dysfunction are found in the early stages of pregnancy in women who later on develop preeclampsia. Appropriate prenatal care programs, including screening and treatment of urinary, vaginal, and periodontal infections in early pregnancy and prevention of factors that predispose to insulin resistance, such as excessive weight gain during pregnancy, may reduce the incidence of preeclampsia in Latin-American women.