Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.4 (SOR)
 720 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that the severity of experimentally induced acute renal failure (ARF) is inversely related to dietary sodium chloride intake, and the effects have been attributed to the concurrent changes in renal renin. In the current study, renal renin of rats was increased by chronic sodium deprivation and decreased by chronic sodium loading and DOCA administration. In two nephrotoxic models (mercuric chloride, uranyl nitrate), giving previously sodium-deprived rats 1% sodium chloride to drink for 48 hours prior to ARF induction greatly attenuated the severity without any reduction in their high renal renin. Conversely, giving previously sodium-loaded rats tap water to drink for 4 to 5 days prior to AFR induction greatly enhanced the severity without any increase in their subnormal renal renin. Therefore, the changes in severity of ARF resulting from changes in dietary sodium are not mediated by changes in renal renin. Significant inverse correlations were found between mean peak BUN values during the follow-up period (5 to 7 days) and the 24-hour urinary sodium excretions prior to ARF induction in both models, suggesting that sodium intake and/or excretion at the time of induction is a good predictor of the severity. The effects of sodium chloride in both models were predominantly expressed during the maintenance phase, and consisted of attenuation of the severity (both models) and hastening of the recovery (mercuric chloride model). Possible mechanisms by which dietary sodium produced its effects, independently of its effects on the renin-angiotensin system, are discussed.
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PMID:Sodium-chloride-induced protection in nephrotoxic acute renal failure: independence from renin. 39 16

We examined the effect of 1% L-arginine in the drinking water on the infiltration of the kidney by macrophages in rats with puromycin aminonucleoside-induced nephrosis (PAN) and in rats with bilateral ureteral obstruction (BUO) of 24 hours duration. Rats given L-arginine in the drinking water for three days before BUO or PAN was initiated had a greater glomerular filtration rate after release of BUO or induction of PAN than similar rats not given L-arginine (P < 0.0001). Administration of L-arginine decreased the renal infiltration by macrophages in rats with PAN (P < 0.0001) or BUO (P < 0.0001) compared to rats with PAN or BUO given tap water alone. Chemotaxis studies suggested that macrophages were activated during obstruction as evidenced by the greater random migration of peritoneal macrophages obtained from rats with 24-hour urethral obstruction than from sham-operated rats (SOR; P < 0.0001). In vitro, maximal chemotaxis induced by 7% zymosan-activated serum (ZAS) in peritoneal macrophages from SOR was enhanced by low (10(-6) to 10(-5) M) and decreased by high concentrations (10(-3) to 10(-2) M) of L-arginine in the incubation medium. Migration of macrophages from rats with urethral obstruction was increased by 7% ZAS but the increase diminished with high concentrations of L-arginine (10(-3) to 10(-2) M). Random migration of peritoneal macrophages obtained from rats with urethral obstruction given L-arginine prior to obstruction was significantly lower than that of peritoneal macrophages obtained from similar rats given tap water alone prior to obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:L-arginine decreases the infiltration of the kidney by macrophages in obstructive nephropathy and puromycin-induced nephrosis. 807 47