Browsing by Author "Valdes, Gloria"

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    ACE2 and ANG-(1-7) in the rat uterus during early and late gestation
    (AMER PHYSIOLOGICAL SOC, 2008) Neves, Liomar A. A.; Stovall, Kathryn; Joyner, JaNae; Valdes, Gloria; Gallagher, Patricia E.; Ferrario, Carlos M.; Merrill, David C.; Brosnihan, K. Bridget
    The present study was designed to determine ANG peptide content [ANG I, ANG II, ANG( 1-7)], ACE2 mRNA, and the immunocytochemical distribution of ANG-(1-7) and ACE2 in the uteroembryonic unit during early and late gestation in Sprague-Dawley rats and in a rat model of pregnancy-induced hypertension, the reduced uterine perfusion pressure (RUPP) model. At early pregnancy ANG-(1-7) and ACE2 staining were localized in the primary and secondary decidual zone and luminal and glandular epithelial cells. During late gestation, ANG-(1-7) and ACE2 staining was visualized in the labyrinth placenta and amniotic and yolk sac epithelium. Uterine ANG II concentration at early pregnancy was significantly decreased by 21-55% in the implantation and interimplantation sites compared with virgin rats, whereas ANG-(1-7) levels were maintained at prepregnancy levels. At late gestation, uterine concentrations of ANG I and ANG II were significantly increased (30% and 25%, respectively). In RUPP animals, ANG-(1-7) concentration is significantly reduced in the uterus (181 +/- 16 vs. 372 +/- 74 fmol/g of tissue) and placenta (143 +/- 26 vs. 197 +/- 20 fmol/g of tissue). ACE2 mRNA increased in the uterus of early pregnant compared with virgin rats, yet within the implantation site it was downregulated. At late pregnancy, ACE2 mRNA is elevated by 58% in the uterus and decreased by 59% in RUPP animals. The regulation of ANG-(1-7) and ACE2 in early and late pregnancy supports the hypothesis that ANG-(1-7) and ACE2 may act as a local autocrine/paracrine regulator throughout pregnancy, participating in the early (angiogenesis, apoptosis, and growth) and late (uteroplacental blood flow) events of pregnancy.
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    Association of adrenal medullar and cortical nodular hyperplasia - A report of two cases with clinical and morpho-functional considerations
    (HUMANA PRESS INC, 2006) Valdes, Gloria; Roessler, Eric; Salazar, Ivan; Rosenberg, Helmar; Fardella, Carlos; Martinez, Pedro; Velasco, Alfredo; Velasco, Soledad; Orellana, Pilar
    Arterial hypertension of adrenal etiology is mainly attributed to primary hyperaldosteronism. However, subtle expressions of hyperadrenergic or glucocorticoid excess can also generate arterial hypertension. The present report describes two hypertensive patients cataloged as resistant essential hypertensives, in whom adrenal masses were found incidentally, who highlight the need to recognize these tenuous clinical or laboratory presentations. Case 1 was a 50-yr-old female with hyperadrenergic hypertension associated to a left adrenal node, normal cortisol and aldosterone:renin ratio, marginally increased urinary normetanephrine, and a positive I-131 MIBG radioisotope scan. Adrenalectomy normalized blood pressure and urinary metanephrines. Pathology showed a hyperplastic adrenal medulla associated to a multinodular cortical hyperplasia. Case 2 was a 62-yr-old female with progressive hypertension, a slight Cushing phenotype, non-suppressible hypercortisolism, normal urinary metanephrines, and bilateral adrenal nodes. Bilateral adrenalectomy and subsequent replacement normalized blood pressure and phenotypic stigmata. Pathology demonstrated bilateral cortical multinodular hyperplasia and medullary hyperplasia. The clinical study in both patients was negative for MEN. The apparently rare association of cortical and medullary lesions presented by both patients is probably overlooked in routine pathology exams, but should be meticulously searched since the crosstalk between the adrenal cortex and medulla may prompt dual abnormalities.
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    Association of Remote Hypertension in Pregnancy With Coronary Artery Disease A Case-Control Study
    (LIPPINCOTT WILLIAMS & WILKINS, 2009) Valdes, Gloria; Quezada, Felipe; Marchant, Eugenio; von Schultzendorff, Astrid; Moran, Sergio; Padilla, Oslando; Martinez, Alejandro
    Because hypertensive pregnancies have been associated with increased cardiovascular disease, we aimed to identify whether angiographically characterized coronary artery disease differed in women with previous normotensive pregnancies or hypertensive pregnancies (HPs). The study group included 217 parous women, aged 60.9 +/- 9.2 (SD) years, who required coronary angiography between January 2006 and December 2007, 36.8 +/- 9.9 and 28.8 +/- 10.5 years after their first and last pregnancy, respectively; 146 had normotensive pregnancies and 71 had >= 1 HP, according to a questionnaire including reproductive history and cardiovascular risks. Body mass index, smoking, and frequency of diabetes were similar in both groups. Chronic hypertension (93% versus 78%; P=0.007), hyperlipidemia (82% versus 69%; P=0.049), and premature familial cardiovascular disease (42% versus 20%; P=0.001) prevailed in HPs. Participants with HPs were younger (58.9 +/- 8.3 versus 61.9 +/- 9.6 years; P=0.025) than participants with normotensive pregnancies. Although 49% of all participants had hemodynamically significant coronary artery disease (>= 70% stenosis), no differences were observed between groups in the number of stenotic arteries; however, their number increased by 28% and 22% over a 10-year period in HPs and normotensive pregnancies, respectively (P=0.034). Multivariate analysis showed that HPs had a nonsignificant risk of having coronary artery disease (odds ratio: 1.21; 95% CI: 0.64 to 2.28), and being a current smoker (odds ratio: 4.13; 95% CI: 1.85 to 9.25), a diabetic (odds ratio: 2.29; 95% CI: 1.85 to 9.25), or having a family history of premature cardiovascular disease (odds ratio: 2.34; 95% CI: 1.17 to 2.39) significantly increased the risk of coronary artery disease. This study demonstrates that women with HPs have earlier coronary disease, probably related to intermediate cardiovascular risks that have a gestational expression. (Hypertension. 2009; 53: 733-738.)
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    Clinical Presentation and Perioperative Management of Pheochromocytomas and Paragangliomas: A 4-Decade Experience
    (ENDOCRINE SOC, 2021) Uslar, Thomas; San Francisco, Ignacio F.; Olmos, Roberto; Macchiavelo, Stefano; Zuniga, Alvaro; Rojas, Pablo; Garrido, Marcelo; Huete, Alvaro; Mendez, Gonzalo P.; Cortinez, Ignacio; Zemelman, Jose Tomas; Cifuentes, Joaquin; Castro, Fernando; Olivari, Daniela; Dominguez, Jose Miguel; Arteaga, Eugenio; Fardella, Carlos E.; Valdes, Gloria; Tagle, Rodrigo; Baudrand, Rene
    Purpose: Latin American reports on pheochromocytomas and paragangliomas (PPGLs) are scarce. Recent studies demonstrate changes in clinical presentation and management of these patients. Herein, we assessed the main characteristics of PPGL patients in our academic center over the past 4 decades.
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    Endothelial dysfunction - A link among preeclampsia, recurrent pregnancy loss, and future cardiovascular events?
    (LIPPINCOTT WILLIAMS & WILKINS, 2007) Germain, Alfredo M.; Romanik, Mary Carmen; Guerra, Irene; Solari, Sandra; Soledad Reyes, Maria; Johnson, Richard J.; Price, Karen; Karumanchi, S. Ananth; Valdes, Gloria
    We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, L-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n = 22), patients with severe preeclampsia (n = 25), or patients with recurrent pregnancy loss (n = 29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, L-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated.