[Excretory function of the kidney after denervation and the administration of a beta-blockader].
Osmotic diuresis (15% mannitol, 4.5 ml/hr) was in duced in anesthetized rats. At the end of each of 10 consecutive 10-min clearance periods the following parameters were determined: diuresis, sodium, chlorine and osmotic excretion, GFR (inulin clearance). The animals were divided into three groups: a) controls, b) with bilateral renal denervation (performed one week earlier) and c) with application of beta-adrenergic blocking agent propranolol (Obsidan, Germed DDR) introduced intravenously 0.1 mg/100 g initially and 0.12 mg/100 g sustaining dose during 2 hrs. The experimental results showed an increased sodium excretion in denervated and obsidan--treated animals with no change of the total excreted osmotically active substances. In denervated animals the chlorine excretion was increased as well. The data suggest that, in osmotic diuresis, the renal denervation and beta-adrenergic blocking agents inhibit the tubular sodium transport. The kidney osmoregulatory functions remains unchanged.
[Excretory function of the kidney after denervation and the administration of a beta-blockader]. Osmotic diuresis (15% mannitol, 4.5 ml/hr) was in duced in anesthetized rats. At the end of each of 10 consecutive 10-min clearance periods the following parameters were determined: diuresis, sodium, chlorine and osmotic excretion, GFR (inulin clearance). The animals were divided into three groups: a) controls, b) with bilateral renal denervation (performed one week earlier) and c) with application of beta-adrenergic blocking agent propranolol (Obsidan, Germed DDR) introduced intravenously 0.1 mg/100 g initially and 0.12 mg/100 g sustaining dose during 2 hrs. The experimental results showed an increased sodium excretion in denervated and obsidan--treated animals with no change of the total excreted osmotically active substances. In denervated animals the chlorine excretion was increased as well. The data suggest that, in osmotic diuresis, the renal denervation and beta-adrenergic blocking agents inhibit the tubular sodium transport. The kidney osmoregulatory functions remains unchanged.