Browsing by Author "Gonzalez, Alexis A."

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    A polymorphic GT short tandem repeat affecting beta-ENaC mRHA expression is associated with low renin essential hypertension
    (OXFORD UNIV PRESS, 2007) Gonzalez, Alexis A.; Carvajal, Cristian A.; Riquelme, Erick; Krall, Paola M.; Munoz, Carlos R.; Mosso, Lorena M.; Kalergis, Alexis M.; Fardella, Carlos E.
    Background: The epithelial sodium channel (ENaC) is a candidate gene associated with the development of essential hypertension. A potentially polymorphic repetitive region (GT dinucleotide short tandem repeat [STR]) was identified in intron 8 of beta-ENaC gene (SCNN I B). The aim of this study was to identify the prevalence and distribution of a polymorphic GT-STR in SCNN1B in Chilean essential hypertensive (EH) patients and to analyze the correlation between the different genotypes with plasma renin activity (PRA) and serum aldosterone (SA), and furthermore, to evaluate the beta-ENaC gene expression in vitro.
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    Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure
    (SOC BIOLGIA CHILE, 2012) Villanueva, Sandra; Escobar, Pia; Jacubovsky, Ioram; Irarrazabal, Carlos; Carreno, Juan E.; Erpel, Jose M.; Cespedes, Carlos; Gonzalez, Alexis A.; Vio, Carlos P.; Velarde, Victoria
    Acute renal failure (ARF) can be caused by injuries that induce tissue hypoxia, which in turn can trigger adaptive or inflammatory responses. We previously showed the participation of basic fibroblast growth factor (FGF-2) in renal repair. Based on this, the aim of this study was to analyze the effect of FGF-2 signaling pathway manipulation at hypoxia-induced protein levels, as well as in key proteins from the vasoactive systems of the kidney. We injected rat kidneys with FGF-2 recombinant protein (r-FGF) or FGF-2 receptor antisense oligonucleotide (FGFR2-ASO) after bilateral ischemia, and evaluated the presence of iNOS, EPO and HO-1, in representation of hypoxia-induced proteins, as well as COX-2, renin, kallikrein, and B2KR, in representation of the vasoactive systems of the kidney. A reduction in iNOS, HO-1, EPO, renin, kallikrein, B2KR, and in renal damage was observed in animals treated with r-FGF. The opposite effect was found with FGF-2 receptor down-regulation. In contrast, COX-2 protein levels were higher in kidneys treated with r-FGF and lower in those that received FGFR2-ASO, as compared to saline treated kidneys. These results suggest that the protective role of FGF-2 in the pathogenesis of ARF induced by I/R is a complex process, through which a differential regulation of metabolic pathways takes place.
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    E Prostanoid-1 receptor regulates renal medullary αENaC in rats infused with angiotensin II
    (2009) Gonzalez, Alexis A.; Cespedes, Carlos; Villanueva, Sandra; Michea, Luis; Vio, Carlos P.
    E Prostanoid (EP) receptors play an important role in urinary Na+ excretion. In the kidney, the epithelial sodium channel (ENaC) is the rate-limiting-step for Na+ reabsorption. We hypothesized that activation of EP1/EP3 regulates the expression of ENaC in the face of renin-angiotensin-aldosterone-system (RAAS) activation. In primary cultures of inner medullary collecting duct (IMCD) cells, sulprostone (EP1 > EP3 agonist, 1 mu M) and 17 Phenyl trinor (17 Pt, EP1 agonist, 10 mu M) prevented the up-regulation of alpha ENaC mRNA induced by aldosterone (10 nM). In Sprague-Dawley rats infused with angiotensin II (0.4 mu g/kg/min), alpha ENaC expression was up-regulated in renal cortex and medulla coincidently with high plasma aldosterone levels. Sulprostone and/or 17 Pt prevented this effect in renal medulla but not in cortex. Immunocytochemistry demonstrated that IMCD cells express EP1. Our results suggest that specific activation of EP1 receptor during RAAS activation antagonizes the action of aldosterone on alpha ENaC expression in the renal medulla. (C) 2009 Elsevier Inc. All rights reserved.