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The renal function has been evaluated by clearance (cl.) method during hypotonic polyuria and successive moderate antidiuresis induced by a low dose of lysine-8-vasopressin; four 15 min and two 60 min cl. periods were performed, respectively. Glomerular filtration rate was estimated by creatinine cl.; the osmotic cl. (Cosm, CH2O), the absolute and fractional excretions of water, sodium, potassium and chloride were determined by usual methods. The urinary concentrations of PGE2, 6-keto-PGF1 alpha (6KPGF) and TxB2 were measured by RIA. The study protocol was applied in normal potassium balance and experimental potassium balance (KD), both in absence and presence of indomethacin. In KD groups with a potassium cumulative deficit of 198.4 +/- 22.2 meq (D3; n = 6) during polyuria significant correlations are consistent with the hypothesis that the lower the plasma potassium concentration is the higher the urinary chloride excretion and the inhibition of distal fractional chloride reabsorption. Moreover, by utilizing the polyuria and antidiuresis data pool, the effects of urine flow rate changes on PGE2 and 6KPGF urinary excretions are blunted as compared to normal potassium balance (n = 14). After indomethacin treatment (D3.I) the following functional relationships are disclosed: a) the lower the kaliemia is the lower the urinary chloride and potassium excretions and the higher the fractional isosmotic reabsorption; b) the lower the urinary potassium excretion is the lower the urinary chloride excretion. In both D3 and D3.I experimental groups the positive correlation between urinary chloride excretion and urinary potassium excretion is significant.

We have observed that in the presence of salt retention (DOCA pretreatment) dopamine (DA) promoted a hydro-natriuretic effect; in contrast in salt depletion (natriuretic pretreatment) the changes in sodium tubular reabsorption and in urinary flow were non significant. The present study was designed to identify the possible mechanisms underlying the hydro-natriuretic effect. DA was infused at a subpressor rate (0,1 microgram/kg . min) during induced hypotonic polyuria. 19 healthy human subjects at different degree of salt retention were studied. The results demonstrate that the tubular inhibitory effects produced by DA on the % sodium reabsorptions (total as % of sodium filtered load, anisosmotic as % of sodium distal load) are the higher the lower are the control values of these reabsorptions. Hence DA appears to act by enhancing the inhibitory tubular response elicited by salt retention. Moreover these inhibitory effects are positively related with the simultaneous DA-induced haemodynamic effects. This suggests that the decrease in sodium reabsorptions during DA infusion is haemodynamically mediated.

Type IV Renal tubular acidosis (RTA) is a syndrome whose physiopathological and clinical peculiarities have been described in the last decade. This syndrome can be associated with several pathological conditions characterized by reduced aldosterone activity of which hyporeninemic hypoaldosteronism is the most frequent. Type IV RTA originates in a defect in the distal nephron responsible for hydrogen and kalium ion secretion. Renal hyperchloremic acidosis and hyperkalemia are evident; the net acid secretion is decreased especially because of the urinary reduction in ammonia. Besides the behaviour of the spontaneous humoral parameters, the diagnosis of RTA is based on the tests that explore distal nephron acidification.