Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelium-derived nitric oxide (EDNO) maintains RBF in normal kidneys and to the nonclipped kidney of two-kidney, one-clip (2K, 1C) renovascular hypertensive rats. However, in clipped kidneys with severe renal stenosis, EDNO has been reported not to influence RBF, and it was suggested that low perfusion diminishes the stimulus of shear stress for EDNO synthesis. It was hypothesized that lesser degrees of renal artery stenosis would allow greater renal perfusion and, hence, a greater role for EDNO in maintaining RBF in the clipped kidney. The renal response to EDNO synthesis inhibition was studied with 10 mg/kg body wt N omega-nitro-L-arginine methyl ester (L-NAME). Four weeks after clipping, rats had different degrees of (functional) renal artery stenosis as determined by the ratio (R) of RBF (per gram kidney weight) in the nonclipped to clipped kidney. Stenosis was classified as either mild (R < or = 1.25) or moderate (R > or = 1.30). Both groups were similarly hypertensive (146 +/- 3 versus 148 +/- 6 mm Hg, respectively) and responded to L-NAME with a 42 mm Hg rise in blood pressure. In 2K,1C rats with mild renal artery stenosis, the renal response to L-NAME was similar in both nonclipped and clipped kidneys. RBF decreased by 17 to 19% (P < 0.005) and renal vascular resistance (RVR) increased by 59 to 63% (P < 0.005). When renal perfusion pressure was controlled, the decrease in RBF was exaggerated 3.6-fold in the nonclipped but only 2.3-fold in the clipped kidney, whereas the RVR increased proportionally.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Degree of renal artery stenosis alters nitric oxide regulation of renal hemodynamics. 789 4

Surgical correction of renal artery stenosis in Goldblatt hypertension rapidly normalizes blood pressure and increases renal function. This study was conducted in 1-kidney, 1 clip (1K1C) Goldblatt hypertensive rats to examine whether the unclipping-induced reversal of blood pressure and renal function is mediated by nitric oxide (NO). The 1K1C rats were prepared and given tap water with or without supplementation of NG-nitro-L-arginine methyl ester (L-NAME). Systolic blood pressure (SBP) before and after renal artery clipping was measured with the tail-cuff method. Four weeks later, surgical unclipping was performed while blood pressure and renal function responses were determined. The results show that clipping the renal artery for 4 weeks increased SBP from 140+/-5 to 183+/-6 mm Hg (P<0.05). Concurrent L-NAME treatment accelerated and aggravated the clipping-induced increases in SBP from 138+/-6 to 219+/-8 mm Hg (P<0.05). Surgical unclipping reduced blood pressure to normotensive levels within 2 hours in all hypertensive rats with and without chronic or acute L-NAME treatment. However, the magnitude of reductions in blood pressure in the initial 1 hour after unclipping was significantly less in L-NAME-treated rats than in nontreated rats (9+/-2% versus 16+/-1%, P<0.05). Despite reducing blood pressure, unclipping significantly increased glomerular filtration rate, urine flow, and sodium and potassium excretions, but the extent of the increases in these renal functions was significantly attenuated in L-NAME-treated rats. These data suggest that NO production partly contributes to the hypotensive and renal responses to unclipping but does not mediate the reversal of renovascular hypertension of this model.
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PMID:Nitric oxide synthesis inhibition retards surgical reversal of one-kidney Goldblatt hypertension in rats. 974 Jun 22