ABSTRACT
Epidemiological and experimental studies have led to the hypothesis of the fetal origin of adult diseases, suggesting that some adult diseases might be determined before birth by altered fetal development. Maternal diabetes subjects the fetus to an adverse environment that has been demonstrated to result in metabolic, cardiovascular and renal impairment in the offspring. The growing amount of obesity in young females in developed and some developing countries should contribute to increasing the incidence of diabetes among pregnant women. In this review, we discuss how renal and extrarenal mechanisms participate in the genesis of hypertension induced by a diabetic status during fetal development.
Subject(s)
Animals , Female , Humans , Mice , Pregnancy , Rats , Diabetes Mellitus , Hypertension/embryology , Pregnancy in Diabetics , Diabetes Mellitus/metabolism , Kidney/metabolism , Kidney/physiopathology , Nitric Oxide/biosynthesis , Pregnancy in Diabetics/metabolism , Risk Factors , Renin-Angiotensin System/physiology , Sodium/metabolismABSTRACT
the respone of juvenile cultivated Piaractus mesopotamicus to handling stress, whthout anesthesia, was determined over 3-5 min (T1), 1 h (T2) and 6 h (T3) afeter capture. Plasma cortisol, glucose and total cholesterol were measured. Hyperglycemia present at T2 continued to rise until T3 while plasma cortisol levels increased but were similar at T2 and T3. Total plasma cholesterol was altered only at T3. Hyperglycemic changes were greater in fish without than stomach contents during the T2-T3 period. These differences in hyperglycemic changes may reflect the role of hormones other than cortisol in the regulation of glucose release in these fish
Subject(s)
Rats , Animals , Male , Kainic Acid/pharmacology , Kidney/drug effects , Seizures/chemically induced , Inulin/metabolism , Kidney Function Tests , Glomerular Filtration RateABSTRACT
Acute metabolic acidosis potentiates the nephrotixicity of aminoglycosides by impairing the adequate excretion of ammonium and titratable acidity. The present study assesses distal tubular function after aminoglycoside administration in the rat. Two aminoglycosides, gentamicin and netilmicin were given to rats either in low doses equivalent to those used clinically (BG4 and BN5 groups) or in doses ten times higher (BG40 and BN50). The rats were subjected to acute metabolic alkalosis and the pCO2 of urine was continuously evaluated. the regression lines obtained by plotting the differences between urine and blood pCO2 as a function of urinary HCO3 in low dose models were simsilar to those obtained for the control group. However, the slopes obtained for BG40 and BN50 were significantly different from the control, suggesting an impairment of H+ secretion