Oxygen-dependent inhibition of respiration in isolated renal tubules by nitric oxide
Autor: | Matteus Froelich, Ari Koivisto, Janos Pittner, A. Erik G. Persson |
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Rok vydání: | 1999 |
Předmět: |
Male
aerobic respiration medicine.medical_specialty Kidney Cortex Cellular respiration Cell Respiration adenosine triphosphate chemistry.chemical_element medullary PO2 Mitochondrion Biology In Vitro Techniques Nitric Oxide Oxygen Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Oxygen Consumption Internal medicine Respiration medicine Animals Kidney Kidney Medulla hypoxia renal metabolism renal oxygen Hypoxia (medical) Rats Endocrinology medicine.anatomical_structure Kidney Tubules chemistry Rats Inbred Lew Nephrology Female medicine.symptom Sodium-Potassium-Exchanging ATPase Adenosine triphosphate |
Zdroj: | Kidney International. 55(6):2368-2375 |
ISSN: | 0085-2538 |
DOI: | 10.1046/j.1523-1755.1999.00474.x |
Popis: | Oxygen-dependent inhibition of respiration in isolated renal tubules by nitric oxide. Background The partial pressure (tension) of oxygen (P O 2 ) in the kidney medulla has been established to be lower than that of the cortex. The kidney medulla has been shown to be particularly sensitive to hypoxia. However, the measured P O 2 in the kidney medulla is sufficient to support maximal respiration. It has been recently shown that endogenously produced nitric oxide (NO) may inhibit oxygen consumption in the kidney. We studied whether NO plays a role in hypersensitivity of the kidney medulla to hypoxia. Methods We studied the effect of added NO on isolated cortical and outer medullary renal tubules in simultaneous oxygen consumption and NO measurements at different oxygen concentrations. Results We found that NO could potently and reversibly inhibit respiration at nanomolar concentrations. The inhibitory effect of NO was markedly increased at low physiological oxygen concentrations. The effect of NO was cGMP independent because the selective guanylyl cyclase inhibitor 1H- 1,2,4 oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) at a 10 μm concentration had no effect on basal or NO-inhibited respiration. The value for half-maximal NO-mediated inhibition of respiration was virtually identical to that found in isolated mitochondria, and therefore, NO was most likely directly acting on mitochondria. Interestingly, we found no differences in sensitivity to NO-mediated inhibition between outer medullary and cortical tubules. Conclusions We suggest that because of its low P O 2 , the renal outer medulla is more sensitive to hypoxia, not because of the low P O 2 as such, but probably because of the competition between NO and oxygen to control respiration. |
Databáze: | OpenAIRE |
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