Abstract

Objective: Nitric oxide (NO) plays an important role in renal hemodynamics. We investigated the influence of dietary sodium on renal blood flow and renal NO-synthesis, by determining renal levels of NO inhibitors asymmetric dimethylarginine (ADMA) and L-NG-monomethylarginine (L-NMMA), ADMAs isoform symmetric dimethylarginine (SDMA), NO-precursor l-arginine and NO co-product citrulline. Design and Methods: We included 133 moderately hypertensive patients (all Caucasian) who were scheduled for renal angiography on suspicion of renal artery stenosis, mostly because of resistant hypertension. Patients with renal artery stenosis, fibromuscular dysplasia or proteinuria were excluded. Patients were assigned to adhere to either a sodium-rich diet (>200 mmol/24 h) (n = 56) or a sodium-restricted diet (<55 mmol/24 h) (n = 57) during the week preceding the study. All antihypertensive medication was discontinued 3 weeks before the study. After an overnight fast, patients consecutively underwent selective blood sampling from the aorta and both renal veins, renal flow measurements using 133Xenon washout and renal angiography. In the obtained blood samples we determined levels of ADMA, SDMA, L-NMMA, l-arginine and citrulline (all using high-performance liquid chromatography) and levels of creatinine and renin (using standard methods). 24 h urine was collected to determine urinary sodium excretion. Results: There were no significant differences in renal arterial and renal venous levels of ADMA, SDMA, L-NMMA, l-arginine, citrulline, creatinine and renin between both groups. Neither were there differences in blood pressure or renal blood flow. Renal elimination of ADMA and L-NMMA however, was significantly lower in the high sodium group compared to the low sodium group (11.6% vs. 14.6 %; p = 0.031 and 0.7% vs. 7.6%; p = 0.033 respectively). There was no significant correlation between 24 h urinary sodium excretion and any of the studied parameters. Conclusion: In hypertensive Caucasians, short-term moderate-high dietary sodium does not influence renal blood flow or intrarenal levels of arginines. However, renal elimination of ADMA and L-NMMA is significantly lower in comparison to a low sodium diet, which may result in long-term renal NO-inhibition.

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