The role of nitric oxide in radiation nephropathy. Arch Physiol Biochem 1996;104(2):200-6
Date
01/01/1996Pubmed ID
8818205DOI
10.1076/apab.104.2.200.12880Scopus ID
2-s2.0-0029947763 (requires institutional sign-in at Scopus site) 24 CitationsAbstract
Sufficient radiation will cause kidney injury with hypertension, azotemia, and death from renal failure. There is early endothelial injury after radiation, which could lead to a deficit of constitutive nitric oxide (NO) synthesis, with capillary thrombosis and hypertension, both of which are seen in radiation nephropathy. In a rat radiation nephropathy model, the serial evolution of urinary cyclic guanosine monophosphate (cGMP), a marker of kidney NO, was studied and a deficit in urinary cGMP was found. This radiation-induced cGMP deficit was prevented by high-dose Captopril treatment. Low-dose Captopril treatment protected against radiation nephropathy without preventing the decrease in urinary cGMP. An inhibitor of NO synthesis, L-N-arginine-methylester, did not blunt the beneficial effect of Captopril treatment. We conclude that there is a deficit in urinary cGMP in radiation nephropathy, but that prevention of this deficit is not essential in the prevention of radiation nephropathy by Captopril.
Author List
Cohen EP, Fish BL, Moulder JEMESH terms used to index this publication - Major topics in bold
AnimalsBone Marrow Transplantation
Captopril
Cyclic GMP
Drug Evaluation, Preclinical
Enzyme Inhibitors
Kidney
Male
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Synthase
Pilot Projects
Radiation Injuries, Experimental
Radiation-Protective Agents
Rats
Rats, Inbred Strains
Transplantation, Isogeneic
Whole-Body Irradiation