In this study, rats recovering from glycerol-induced acute renal failure were found to be protected from mercury-induced nephropathy, and HgCl₂ poisoning protected rats from developing myohemoglobinuric renal failure. In view of the widely disparate nature of the renal failure models used, refractoriness appears to relate to an altered sensitivity of the organism itself rather than reflecting resistance to a particular nephropathic challenge. Renal renin content of the rats at the time of rechallenge was normal or high, a finding which contrasts sharply with that of chronically saline-loaded animals which also are refractory to ARF but have a maximally suppressed renal renin content. Renal renin depletion is not essential to the prevention of acute renal failure in the rat.

No abstract

No abstract

The absence of a reduction in peripheral vascular resistance secondary to hypervolaemia leads to so-called volume hypertension. In order to study whether a deficient formation of the vasodilator autacoid prostaglandin E2 (PGE2) contributes to the preservation of inadequate vascular tone during extracellular volume expansion, arterial plasma PGE2 and the stable PGE2 metabolite 13,14-dihydro-15-keto-PGE2 (PGE2-M) were determined in 13 oligoanuric women on chronic haemodialysis. Prior to treatment eight of them had hypervolaemia and hypertension (mean arterial pressure (MAP) 128 +/- 3 mmHg (mean +/- SE] and five patients had hypervolaemia of a similar degree but were not hypertensive (MAP: 99 +/- 4 mmHg P less than 0.005). Before haemodialysis the arterial PGE2 and PGE2-M concentrations were less (P less than 0.05) in hypertensive (11 observations in eight patients) than in normotensive patients (ten observations in five patients). As blood pressure decreased during the course of haemodialysis of volume hypertensive patients, the concentration of PGE2 and PGE2-M increased (P less than 0.02) by 104 +/- 43% and 89 +/- 32%, respectively. In normotensive patients neither blood pressure nor the concentration of PGE2 and PGE2-M were found to change during treatment. Since volume hypertension was associated with reduced values and dialysis induced normalisation of blood pressure with increased arterial values of PGE2 and PGE2-M, we hypothesise that the development of hypertension associated with fluid overload of haemodialysed patients may be related to a decreased release of prostaglandin E2.

No abstract