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Articles by A. G Garcia
Total Records ( 6 ) for A. G Garcia
  D. S De Silva , R. M Wilson , C Hutchinson , P. C Ip , A. G Garcia , S Lancel , M Ito , D. R Pimentel and F. Sam

Aldosterone induces extracellular signal-regulated kinase (ERK)-dependent cardiac remodeling. Fenofibrate improves cardiac remodeling in adult rat ventricular myocytes (ARVM) partly via inhibition of aldosterone-induced ERK1/2 phosphorylation and inhibition of matrix metalloproteinases. We sought to determine whether aldosterone caused apoptosis in cultured ARVM and whether fenofibrate ameliorated the apoptosis. Aldosterone (1 µM) induced apoptosis by increasing terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL)-positive nuclei in ARVM. Spironolactone (100 nM), an aldosterone receptor antagonist, but not RU-486, a glucocorticoid receptor, inhibited aldosterone-mediated apoptosis, indicating that the mineralocorticoid receptor (MR) plays a role. SP-600125 (3 µM)—a selective inhibitor of c-Jun NH2-terminal kinase (JNK)—inhibited aldosterone-induced apoptosis in ARVM. Although aldosterone increased the expression of both stress-activated protein kinases, pretreatment with fenofibrate (10 µM) decreased aldosterone-mediated apoptosis by inhibiting only JNK phosphorylation and the aldosterone-induced increases in Bax, p53, and cleaved caspase-3 and decreases in Bcl-2 protein expression in ARVM. In vivo studies demonstrated that chronic fenofibrate (100 mg·kg body wt–1·day–1) inhibited myocardial Bax and increased Bcl-2 expression in aldosterone-induced cardiac hypertrophy. Similarly, eplerenone, a selective MR inhibitor, used in chronic pressure-overload ascending aortic constriction inhibited myocardial Bax expression but had no effect on Bcl-2 expression. Therefore, involvement of JNK MAPK-dependent mitochondrial death pathway mediates ARVM aldosterone-induced apoptosis and is inhibited by fenofibrate, a peroxisome proliferator-activated receptor (PPAR) ligand. Fenofibrate mediates beneficial effects in cardiac remodeling by inhibiting programmed cell death and the stress-activated kinases.

  C. A Jimenez Ruiz , M. M Ulibarri , N. A Besada , A. C Guerrero , A. G Garcia and A. R. Cuadrado

This uncontrolled study examined the outcome of a program of progressive cigarette reduction, using nicotine gum, as a prelude to complete cessation among 116 smokers (70 men, 46 women; mean age = 45.7 years, SD = 12.65; mean baseline smoking = 28.3 cigarettes/day) who sought treatment in a smokers’ clinic but did not want to quit abruptly.


Subjects participated in a two-stage program consisting of a 4-month reduction phase followed by a 6-month abstinence phase. The aim was to reduce the number of cigarettes smoked daily by at least 50% by Week 8 and to quit at the end of Week 16. During the reduction phase, subjects used nicotine gum (2 or 4 mg) to progressively decrease smoking. During the abstinence phase, subjects used any type of nicotine replacement therapy (NRT) to remain smoke free. Psychological treatment and NRT were provided at no cost to participants.


At Month 2, 76 subjects (68%) achieved the target of 50% reduction. At the target quit date in Week 16, 66 subjects (57%) achieved carbon monoxide–validated abstinence and 45 subjects (39%) maintained continuous abstinence at the 6-month follow-up. No symptoms of nicotine overdose were detected.


A program of progressive cigarette reduction using nicotine gum is feasible in practice and may be a useful strategy for smokers who are unable or unwilling to quit by abrupt cessation.

  J. C Fernandez Morales , L Cortes Gil , A. G Garcia and A. M. G. de Diego

Studies on the bulk catecholamine release from fetal and neonatal rat adrenals, adrenal slices, or isolated chromaffin cells stimulated with high K+, hypoxia, hypercapnia, or acidosis are available. However, a study analyzing the kinetics of quantal secretion is lacking. We report here such a study in which we compare the quantal release of catecholamines from immature rat embryo chromaffin cells (ECCs) and their mothers' (MCCs). Cell challenging with a strong depolarizing stimulus (75 mM K+) caused spike bursts having the following characteristics. ECCs released more multispike events and wave envelopes than MCCs. This, together with narrower single-spike events, a faster decay, and a threefold smaller quantal size suggest a faster secretory machinery in ECCs. Furthermore, with a milder stimulus (25 mM K+) enhanced Ca2+ entry by L-type Ca2+ channel activator BAY K 8644 did not change the kinetic parameters of single spikes in ECCs; in contrast, augmentation of Ca2+ entry increased spike amplitude and width, quantal size, and decay time in MCCs. This suggests that in mature MCCs, the last exocytotic steps are more tightly regulated than in immature ECCs. Finally, we found that quantal secretion was fully controlled by L-type voltage-dependent Ca2+ channels (VDCCs) in ECCs, whereas both L- and non-L VDCCs (N and PQ) contributed equally to secretion control in MCCs. Our results have the following physiological, pharmacological, and clinical relevance: 1) they may help to better understand the regulation of adrenal catecholamine release in response to stress during fetal life and delivery; 2) if clinically used, L-type Ca2+ channel blockers may augment the incidence of sudden infant death syndrome (SIDS); and 3) so-called Ca2+ promotors or activators of Ca2+ entry through L-type VDCCs may be useful to secure a healthy catecholamine surge upon violent stress during fetal life, at birth, or to prevent the SIDS in neonates at risk.

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