Lima A A, Monteiro H S, Fonteles M C
Laboratório de Farmacologia Renal e Metabólica, Faculdade de Medicina, Universidade Federal do Ceará, Fortaleza, CE, Brasil.
Braz J Med Biol Res. 1993 Sep;26(9):983-7.
Cholera toxin peptide stimulates adenylyl cyclase activity in several tissues and causes severe intestinal water and electrolyte secretion. To evaluate the regulatory function of sodium transport in renal tubules, we studied the effect of cholera toxin peptide on rat kidneys. Isolated kidneys from adult male hooded rats weighting 240-335 g were perfused with Krebs-Henseleit solution containing 60 mg/ml dialyzed bovine serum albumin (BSA). The effects of Vibrio cholerae peptide (CT; molecular weight, approximately 82,000 Dalton) on glomerular filtration rate (GFR), proximal sodium reabsorption (%pTNa+) and urinary flow rate (UF) were studied. All experiments were preceded by a 30-min control period and in another group of kidneys the time course of the variables was followed without toxin infusion, for a paired control. Control kidneys perfused with Krebs-Henseleit solution plus 60 mg/ml BSA presented stable GFR (paired internal control GFR30 min = 0.596 +/- 0.248 ml g-1 min-1 vs GFR120 min = 0.694 +/- 0.362, N = 32; P > 0.05) and %pTNa+ (%pTNa+ 30 min = 75 +/- 8.3 vs 84 +/- 1.6 for the internal control, N = 32; P > 0.05). CT caused a dose (0.03, 0.75 and 1.0 microgram/ml)-dependent decrease in GFR starting at 30 min and with a maximal peak of effect at 90 min after toxin infusion (GFRCT = 0.130 +/- 0.086 ml g-1 min-1, N = 12, vs paired internal control GFRControl/30 min = 0.660 +/- 0.132, N = 12; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
