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Published on: July 3, 2013
Nitric oxide and renal protection in morphine-dependent rats
Rouhollah Habibey1, Marjan Ajami, Soltan Ahmed Ebrahimi
1Department of Physiology, Iran University of Medical Sciences, Tehran, Iran.
Free Radical Biology & Medicine
|July 6, 2010
Summary
Morphine dependence protects kidneys from injury by maintaining balanced nitric oxide (NO) production and inducible NO synthase (iNOS) expression. This renal protection is observed during acute treatment and withdrawal phases.
Area of Science:
- Nephrology
- Pharmacology
- Physiology
Background:
- Morphine is known to protect the heart from ischemia-reperfusion (IR) injury.
- The role of nitric oxide (NO) in morphine-induced renal protection remains unclear.
- Kidney injury following IR is a significant clinical concern.
Purpose of the Study:
- To investigate the involvement of nitric oxide (NO) in morphine-induced renal protection against ischemia-reperfusion (IR) injury.
- To evaluate the effects of morphine dependence and withdrawal on renal function and oxidative stress markers.
- To determine the role of balanced NO production and inducible NO synthase (iNOS) expression in morphine's protective effects.
Main Methods:
- Rats were rendered morphine-dependent via chronic administration and then subjected to unilateral kidney IR.
- Renal function was assessed by measuring serum creatinine, blood urea nitrogen (BUN), creatinine clearance, and fractional excretion of sodium (FE(Na)).
- Oxidative stress markers (MPO activity, MDA level), iNOS expression, and histopathology were analyzed in kidney tissue. Naloxone and L-NAME were used as pretreatments.
Main Results:
- Morphine dependence significantly attenuated IR-induced kidney injury, improving renal function and reducing oxidative stress and iNOS expression.
- Pretreatment with naloxone or L-NAME abolished the protective effects of morphine dependence, indicating a crucial role for NO signaling.
- Renal protection persisted during the morphine withdrawal period, with sustained functional improvements despite decreased iNOS expression.
Conclusions:
- Morphine dependence confers significant renal protection against IR injury, both acutely and during withdrawal.
- Balanced nitric oxide (NO) production and inducible NO synthase (iNOS) expression are critical for mediating morphine's renoprotective effects.
- Interference with NO pathways via naloxone or L-NAME negates the protective benefits of morphine dependence.
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