about
Sex hormones in the cardiovascular systemLow-level lead exposure increases systolic arterial pressure and endothelium-derived vasodilator factors in rat aortasAcute lead exposure increases arterial pressure: role of the renin-angiotensin systemEnhanced resistance to permeability transition in interfibrillar cardiac mitochondria in dogs: effects of aging and long-term aldosterone infusionGlucose 6-phosphate dehydrogenase deficiency increases redox stress and moderately accelerates the development of heart failureNa+K+-ATPase activity and K+ channels differently contribute to vascular relaxation in male and female ratsLow mercury concentration produces vasoconstriction, decreases nitric oxide bioavailability and increases oxidative stress in rat conductance artery.Carvedilol prevents ovariectomy-induced myocardial contractile dysfunction in female ratDocosahexaenoic acid supplementation alters key properties of cardiac mitochondria and modestly attenuates development of left ventricular dysfunction in pressure overload-induced heart failureEffect of a high-protein diet on development of heart failure in response to pressure overload.Sex Hormones Promote Opposite Effects on ACE and ACE2 Activity, Hypertrophy and Cardiac Contractility in Spontaneously Hypertensive Rats.Cardiomyocyte deletion of mitofusin-1 leads to mitochondrial fragmentation and improves tolerance to ROS-induced mitochondrial dysfunction and cell deathDietary fat and heart failure: moving from lipotoxicity to lipoprotection.A single resistance exercise session improves myocardial contractility in spontaneously hypertensive ratsEvaluation of docosahexaenoic acid in a dog model of hypertension induced left ventricular hypertrophy.Assessment of cardiac proteome dynamics with heavy water: slower protein synthesis rates in interfibrillar than subsarcolemmal mitochondria.Left and right ventricle late remodeling following myocardial infarction in rats.Cardiac mitochondrial proteome dynamics with heavy water reveals stable rate of mitochondrial protein synthesis in heart failure despite decline in mitochondrial oxidative capacity.Estrogen regulates spatially distinct cardiac mitochondrial subpopulations.Testosterone deficiency prevents left ventricular contractility dysfunction after myocardial infarction.Sex differences in the regulation of spatially distinct cardiac mitochondrial subpopulations.Correction: Sex Hormones Promote Opposite Effects on ACE and ACE2 Activity, Hypertrophy and Cardiac Contractility in Spontaneously Hypertensive Rats.Low-salt diet increases NO bioavailability and COX-2 vasoconstrictor prostanoid production in spontaneously hypertensive rats.Chronic iron overload in rats increases vascular reactivity by increasing oxidative stress and reducing nitric oxide bioavailability.Chronic iron overload induces functional and structural vascular changes in small resistance arteries via NADPH oxidase-dependent O2- production.Vascular activation of K+ channels and Na+-K+ ATPase activity of estrogen-deficient female rats.MitoQ improves mitochondrial dysfunction in heart failure induced by pressure overload.Tributyltin chloride increases phenylephrine-induced contraction and vascular stiffness in mesenteric resistance arteries from female rats.Exercise modulates the aortic renin-angiotensin system independently of estrogen therapy in ovariectomized hypertensive rats.Low-level lead exposure changes endothelial modulation in rat resistance pulmonary arteries.Treatment with high dose of atorvastatin reduces vascular injury in diabetic rats.Activation of K+ channels and Na+/K+ ATPase prevents aortic endothelial dysfunction in 7-day lead-treated ratsVentricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in ratsLinoleic acid reduces vascular reactivity and improves the vascular dysfunction of the small mesentery in hypertension
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description
investigador
@es
researcher
@en
name
Rogerio F Ribeiro
@en
type
label
Rogerio F Ribeiro
@en
prefLabel
Rogerio F Ribeiro
@en
P31
P496
0000-0002-9725-3869