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诱导型一氧化氮合酶与Dahl |
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siological regulator of vascular tone［1，2］. At least three nitric oxide synthases (NOS) including endothelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS) have been clarified so far. Although numerial studies have evidenced that NO derived from eNOS played a key role in the regulation of arterial pressure since NO, as an endothelium derived relaxing factor (EDRF), was firstly reported by Furchgott et al in 1980［1，3，4］, little has been known about the hemodynamic effect of inducible NOS/NO pathway on blood pressure regulation. A lot of reports suggested that the inducible isoenzyme has a very different nature from constitutive NOS including eNOS and nNOS. When exposed to cytokines or bacterial products, iNOS could be greatly activated and produces hundreds or thousands fold NO than it does usually［5～7］. Our previous work showed that the urinary nitrite/nitrate (NO-2/NO-3) excretion (UNOx) and the iNOS expression significantly increased in Sprague-Dawley (SD) rats when feeded with high sodium diet and this results led us suggest that iNOS could play a certain role in the regulation of blood pressure in NaCl-induced hypertension.
In this study, we examined the effect of high sodium chloride (NaCl) infusion on NO production and iNOS activity in renal tissue and the effect of co-infusion of aminoguanidine (AG), a selective inhibitor of iNOS, on hypertensive effect of high NaCl administration in Dahl salt-sensitive rats to clarify the role of iNOS in the regulation of blood pressure.
MATERIALS AND METHODS
In vivo chronical hemodynamic experiment Conscious 7～8 weeks old, male, Dahl salt-sensitive (DS) rats were received when they were 5～6 weeks old, and surgery was done when the rats reached a weight of～200 g, and experiments were begun 1 week later when the rats had a weight of～220 g. Aortic and vena cava catheters were implanted as we have done before［3］, and 15 mL/d of either hypotonic or hypertonic saline was infused iv con上一页 [1] [2] [3] 下一页
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