The roles of nitric oxide (NO) and plasma renin activity (PRA) in the depressor response to chronic administration of Tempol in spontaneously hypertensive rats (SHR) are not clear. The present study was done to determine the effect of 2 wk of Tempol treatment on blood pressure [mean arterial pressure (MAP)], oxidative stress, and PRA in the presence or absence of chronic NO synthase inhibition. SHR were divided into four groups: control, Tempol (1 mmol/l) alone, nitro-L-arginine methyl ester (L-NAME, 4.5 mg x g(-1).day(-1)) alone, and Tempol + L-NAME or 2 wk. With Tempol, MAP decreased by 22%: 191 +/- 3 and 162 +/- 21 mmHg for control and Tempol, respectively (P < 0.05). L-NAME increased MAP by 16% (222 +/- 2 mmHg, P < 0.01), and L-NAME + Tempol abolished the depressor response to Tempol (215 +/- 3 mmHg, P < 0.01). PRA was not affected by Tempol but was increased slightly with L-NAME alone and 4.4-fold with L-NAME + Tempol. Urinary nitrate/nitrite increased with Tempol and decreased with L-NAME and L-NAME + Tempol. Tempol significantly reduced oxidative stress in the presence and absence of L-NAME. In conclusion, in SHR, Tempol administration for 2 wk reduces oxidative stress in the presence or absence of NO, but in the absence of NO, Tempol is unable to reduce MAP. Therefore, NO, but not changes in PRA, plays a major role in the blood pressure-lowering effects of Tempol. These data suggest that, in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress but not blood pressure.

Cardiovascular disease is the leading cause of death in women after menopause. Hypertension, a major cardiovascular risk factor, becomes more prevalent after menopause. The mechanisms responsible for the increase in blood pressure (BP) in postmenopausal women are unknown. We have recently characterized the aged, postestrous-cycling (PMR) spontaneously hypertensive rats (SHR) as a model of postmenopausal hypertension. The purpose of the present study was to determine whether endothelin plays a role in the increased BP in PMR. Premenopausal female SHR, aged 4 -5 mo (YF), and PMR, aged 16 mo, were studied. Expression of preproendothelin-1 mRNA was not different in either renal cortex or medulla between PMR and YF (n ϭ 7-8/group). In contrast, ET-1 peptide expression was significantly higher in renal cortex of PMR than in renal cortex of YF, but there was no difference in medullary ET-1. Expression of endothelin ET A receptor (ETAR) mRNA was lower in renal cortex and medulla of PMR than of YF. Additional groups of rats (n ϭ 6 -7/group) were treated for 3 wk with the ETAR antagonist ABT-627 (5 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ). BP was significantly higher in PMR than in YF. ETAR antagonist reduced BP in PMR by 20% to the level found in control YF. ETAR antagonist had no effect on BP in YF. These data support the hypothesis that the increase in BP in PMR is mediated in part by endothelin and the ET AR. ETA receptor; ETB receptor; kidney AFTER MENOPAUSE, blood pressure (BP) increases in women such that the prevalence of hypertension is higher in postmenopausal women than in age-matched men (5, 24). The reasons why BP increases in women after menopause are not known. However, endothelin has been suggested to play a role in the increase in BP in postmenopausal women because plasma levels of endothelin have been shown to be increased after menopause (15), and hypertensive postmenopausal women have higher endothelin levels than normotensive ones (25).Recently, we characterized a model of postmenopausal hypertension in the aging female spontaneously hypertensive rat (SHR). Throughout their reproductive lives, female SHR have lower BPs than males (17). However, the female SHR stops cycling at 10 -12 mo of age, and, by 16 -18 mo of age, BP levels are similar to or higher than those in age-matched male SHR (11). This loss of the sexual dimorphism in BP is due to an increase in BP in the females rather than any change in BP in the males after 8 mo of age (11). Postcycling female SHR (PMR) also exhibit increases in plasma renin activity, renal vasoconstriction, and renal injury when compared with premenopausal females (11), suggesting that a vasoconstrictor may be involved in the increase in BP in PMR.In the present study, we determined whether endothelin plays a role in mediating postmenopausal hypertension in PMR. Because the kidney is the major long-term controller of BP, we tested the hypothesis of whether there was an increase in the expression of endothelin-1 (ET-1) in the kidneys of PMR compared with young female rats and whether a s...

The authors evaluated 46 patients several hours to 10 years of age and found that in neonates and young infants, the renal cortex is normally as echogenic as the hepatic parenchyma. Within 2 to 3 months, the renal cortex becomes progressively less echogenic than the liver; however, in patients with renal parenchymal disease, cortical echogenicity increases. Sonography is very sensitive to this condition, especially in older children; however, the overall findings are nonspecific. The authors conclude that ultrasound is helpful in screening for renal parenchymal abnormalities in the pediatric patient, since (a) it is very sensitive in the detection of parenchymal disease, particularly in the neonatal period, and (b) older patients demonstrate a direct correlation between parenchymal abnormality and increased cortical echogenicity; this is not possible in the neonate because the renal cortex is normally as echogenic as the liver. However, ultrasound is relatively nonspecific except for renal cystic disease.

In a retrospective study, we identified 55 elderly patients with acute renal failure (ARF) admitted to our hospital during an 8-year period from 1985 to 1993. Information about the etiology, complications, laboratory data, and treatment course were obtained from the clinical history. Of the 200 patients with ARF admitted to the hospital during this period, 28% were patients more than 60 years old (41 male and 14 female) with an average age of 68.5 +/- 7 years. The main causes of ARF were sepsis, volume depletion, low cardiac output, arterial hypotension, nephrotoxicity by antibiotics, and obstructive uropathy. The global mortality of elderly patients with ARF was 53%. The mortality rate of the different types of the ARF were: prerenal 35%, intrinsic 64% (oliguric 76%, nonoliguric 50%), and postrenal 40%. Mortality as a result of sepsis occurred in 18 patients (62%), by cardiovascular disease in 4 patients (13%), by acute respiratory failure in 2 patients (7%), and by other causes in 5 patients (18%). In the cases of sepsis, Pseudomonas was detected in 7 cases (39%), Escherichia coli in 2 cases (11%), Gram-negative nonspecific in 3 cases (17%), Klebsiella in 1 case (5%), and in 5 cases (16%), the hemoculture was negative. The patient survival rate was 47% (26 of 55 patients). Of these patients, 19 recovered their normal renal function (73%), but 7 patients remained with renal failure (27%). In conclusion, the global mortality in the elderly patients without considering the types of ARF was 53%. The oliguric form had the highest mortality rate with 76%. The main causes for mortality were sepsis with 62%, cardiovascular disease with 13%, and other causes 18%.

RESUMEN INTRODUCCIÓN:Se han atribuido muchos efectos beneficiosos a la moringa oleífera en varias publicaciones siendo de gran interés su efecto hipoglicemiante por disminución de la absorción intestinal de glucosa, aunque no está definido si su eficacia hipoglicemiante sería igual o mayor a algún hipoglicemiante oral conocido. El objetivo del presente estudio fue determinar el efecto agudo de moringa oleífera en hiperglucemia inducida por dexametasona en ratas Wistar hembras, así como comparar su efecto hipoglicemiante con la metformina. MATERIALES Y MÉTODOS: Estudio experimental, tres grupos de cinco ratas Wistar hembras, con peso de 188 ± 11 gramos. Se realizó la medición de la glucemia basal con glucómetro, después de 12 horas de ayuno, la inicial al principio del experimento, luego fueron tratadas con dexametasona 10 mg/kg/día, subcutánea, durante 10 días y se tomó la glicemia post dexametasona . Los días 11 a 14, recibieron el grupo 1 (suero fisiológico), grupo 2 (moringa oleífera 300 mg/kg/día) y grupo 3 (metformina 14,28 mg/kp/día), por sonda oro gástrica, el día 15 se tomó la glucemia post tratamiento. Se analizó el promedio, desviación estándar y la correlación mediante la prueba la prueba T de Student, se consideró P < a 0,05 como significativa. RESULTADOS: Grupo 1 (control): glucemia inicial (117 ± 21 mg/dl), post-dexametasona (445 ± 260 mg/dl) y post tratamiento (222 ± 5 mg/dL), Grupo 2 (moringa oleífera): glucemia inicial (95±27 mg/dl), post dexametasona (413 ± 184 mg/dl) y post tratamiento (102 ± 18 mg/dl) y del Grupo 3 (metformina): glucemia inicial (110 ± 5 mg/dl), post-dexametasona (470 ± 146 mg/dl) y post tratamiento (88 ± 11 mg/dL). La glucemia pos tratamiento mostró diferencias entre el grupo 1 y 2 (p < 0,0001), entre el grupo 1 y 3 (p < 0,0001) no hallándose diferencias entre los grupos moringa oleífera y metformina (p = 0,1). DISCUSIÓN: la moringa oleífera disminuye en forma aguda la hiperglucemia inducida por dexametasona en ratas hembras Wistar, con la misma eficacia que la metformina Palabras clave: moringa oleífera, hiperglicemia, ratas Wistar, mefformina. ABSTRACTSanta Cruz F et al  Efecto agudo de moringa oleífera sobre la hiperglucemia inducida por ... An. Fac. Cienc. Méd. (Asunción) / Vol. 48 -Nº 1, 2015 42INTRODUCTION: It has been attributed many beneficial effects of moringa oleífera in various publications to be of great interest for its hypoglycemic effect due to decreased intestinal absorption of glucose; although it is not defined if his hypoglycemic efficacy would be equal to or greater than any known oral hypoglycemic agent. The objective of this study was to determine the acute effect of moringa oleífera on hyperclycemia induced by dexamethasone in female Wistar rats and compare its hypoglycemic effect with metformin. MATERIALS AND METHODS: Experimental study, wiht 3 groups of 5 female Wistar rats, weighing 188 ± 11 grams. Measuring the basal blood glucose meter was performed after 12 hours of fasting, the initial glycemia at the beginning of the experiment and were then ...