Nitric oxide and renal protection in morphine-dependent rats

Habibey, R. and Ajami, M. and Ebrahimi, S.A. and Hesami, A. and Babakoohi, S. and Pazoki-Toroudi, H. (2010) Nitric oxide and renal protection in morphine-dependent rats. Free Radical Biology and Medicine, 49 (6). pp. 1109-1118.

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Abstract

Morphine treatment for 5days protects heart against ischemia-reperfusion (IR) injury. This study evaluated the involvement of nitric oxide (NO) in morphine-induced renal protection. Three weeks after right nephrectomy, increasing doses of morphine were administered (20-30mgkg-1day-1, 5days) to develop dependence in rats. The left kidney underwent 45-min ischemia and 24-h reperfusion. Some rats were pretreated with naloxone (5mgkg-1) or L-NAME (20mgkg-1). In one group, IR was induced 24h after the last dose of morphine during the withdrawal period. Plasma nitrite/nitrate levels and serum creatinine and BUN were measured. Creatinine clearance and fractional excretion of sodium (FENa) were calculated. Myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, and inducible NO synthase (iNOS) expression were determined and histopathology was studied in the left kidney. IR increased serum creatinine and BUN, plasma NO (p<0.01), FENa, iNOS expression (p<0.001), MPO activity, MDA level, and tissue damage and decreased creatinine clearance. Morphine decreased plasma NO (p<0.05 vs IR), serum creatinine and BUN (p<0.01), FENa, MPO activity, MDA level, iNOS expression, and tissue damage (p<0.05), but increased creatinine clearance (p<0.05). Pretreatment with naloxone significantly increased NO production and iNOS expression in morphine-treated rats after IR (p<0.01 vs morphine dependence+IR). Pretreatment with L-NAME in morphine-treated rats decreased NO production (10.7±1.9, p<0.01 vs morphine dependence+IR) but could not change iNOS expression after IR. Both naloxone and L-NAME significantly abolished the protective effects of morphine dependence on functional and histological factors. The protective effect of morphine dependence on serum creatinine, BUN, FENa, and creatinine clearance persisted during the withdrawal period, whereas iNOS expression decreased. NO production was not decreased during the withdrawal period (p>0.1 vs morphine dependence+IR group). Morphine dependence provided renal protection in the acute phase and during withdrawal. Excessive increase or decrease in NO production abolished the effects of morphine, which suggested a role for balanced NO production and iNOS expression. © 2010 Elsevier Inc.

Item Type: Article
Additional Information: cited By 13
Uncontrolled Keywords: creatinine; inducible nitric oxide synthase; malonaldehyde; morphine; myeloperoxidase; n(g) nitroarginine methyl ester; naloxone; nitrate; nitric oxide; nitrite; sodium, animal experiment; animal model; animal tissue; article; blood level; controlled study; creatinine blood level; creatinine clearance; drug dose increase; enzyme activity; histopathology; kidney; kidney ischemia; lipid peroxidation; male; morphine addiction; nephrectomy; nonhuman; oxidative stress; priority journal; protein expression; rat; renal protection; reperfusion injury; signal transduction; single drug dose; sodium urine level; tissue injury; treatment withdrawal; urea nitrogen blood level; urinary excretion, Animals; Blood Urea Nitrogen; Creatinine; Cytoprotection; Kidney; Male; Malondialdehyde; Morphine; Morphine Dependence; Naloxone; Nephrectomy; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase Type II; Peroxidase; Rats; Rats, Wistar; Reperfusion Injury, Rattus
Depositing User: EPrints System Admin
Date Deposited: 19 Jul 2017 10:13
Last Modified: 19 Jul 2017 10:13
URI: http://eprints.iums.ac.ir/id/eprint/46

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