Atrial Natriuretic Peptide Has No Potential to Protect Against Endotoxin-lnduced Acute Renal Failure in the Absence of Renal Nerves.

Abstract

Abstract. Atrial natriuretic peptide (ANP) has been shown to have the potential to restore renal function after ischemic injury, an underlying component of endotoxin (Et)-induced acute renal failure, and is known to counteract renal sympathetic nerve activity in renal function. We have recently found that renal denervation restores the Et-induced renal dysfunction. The purpose of this study was to examine effects of ANP infusion on the Et-induced acute renal failure in the absence of renal nerves. Ten to 14 days after bilateral renal denervation (DNX), Wistar rats (250 to 300 g body wt) were used in the acute experiment.Rats with intact renal nerves (INN) served as controls. Following control clearance measurements, rats were intravenously injected with 4 mg/kg Et (Escherichia coli, 055: B5). During endotoxemia, rats were infused with 10 µg/kg/h ANP or saline vehicle. Et injection reduced the glomerular filtration rate (GFR) significantly in saline-infused INN and DNX rats. ANP infusion restored the greatly reduced GFR to the pre-endotoxemia level in DNX rats but not in INN rats. There was significant difference between the ANP-and saline-infused DNX rats in the percentage change relative to the basal GFR value during the ANP infusion period. ANP infusion did not improve the hyponatriuresis and oliguria after Et administration, which is independent of renal nerves. In conclusion, ANP infusion has a minor reno-protective effect in rats with Et-induced acute renal failure in the absence of the renal nerves.

Prevention and Treatment of Acute Renal Failure in Sepsis

“…In LPS-induced ARF in the rat, urodilatin induced a fall in BP but increased GFR, diuresis, and natriuresis (82). In contrast, ANP did not affect these parameters in a similar model of endotoxemia in the rat (83).…”

Clinical value of natriuretic peptides in chronic kidney disease

“…These changes were accompanied by an early, selective and sustained impaired expression of NPR-A in the renal medulla along with an upregulation of NPR-C in the renal cortex, suggesting a distinct modulation of NPRs in the remnant kidney that could define a possible mechanism for NP resistance in CKD. 34 This could help to explain some of the disappointing results observed both with NP infusion in the renal protection against toxin-induced renal failure and in renal function preservation of patients with decompensated HF 35,36 and limit the clinical use of NP in the treatment of cardio-renal dysfunction.…”

Clinical value of natriuretic peptides in chronic kidney disease

“…34 This could help to explain some of the disappointing results observed both with NP infusion in the renal protection against toxin-induced renal failure and in renal function preservation of patients with decompensated HF 35,36 and limit the clinical use of NP in the treatment of cardio-renal dysfunction. In this study, BP elevation and compromised natriuretic response to VE in ¾nx rats was associated with a precocious and time-dependent increase in circulating BNP levels, in the absence of cardiac dysfunction.…”