Deng X, Welch W J, Wilcox C S
Division of Nephrology, University of Florida, College of Medicine, Gainesville.
Kidney Int. 1994 Sep;46(3):639-46. doi: 10.1038/ki.1994.316.
Since dietary salt loading enhances nitric oxide (NO) generation in the kidney, we investigated the hypothesis that changes in salt intake have specific effects on vascular resistance in the kidney mediated by the L-arginine-NO pathway. We contrasted changes in renal and hindquarter vascular resistances (RVR and HQVR) in anesthetized rats during intravenous infusions of graded doses of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Groups (N = 8 to 10) of rats were maintained on a high salt (HS) or low salt (LS) diet for two weeks. Compared to those on LS, rats on HS had a greater increase in mean arterial pressure (delta MAP; +32 +/- 4 vs. +22 +/- 3%; P = 0.05) and RVR (+160 +/- 17 vs. +83 +/- 10%; P < 0.005) and a greater fall in renal blood flow (delta RBF; -47 +/- 3 vs. -32 +/- 4%; P < 0.01); changes in HQVR were similar in the two groups. The enhanced RVR response to L-NAME in HS rats could not be ascribed to the higher renal perfusion pressure (RPP) since it persisted in rats whose RPP was controlled by adjustment of a suprarenal aortic clamp. Changes in RVR with an NO donor (SIN-1) were similar in HS and LS rats. L-NAME reduced plasma renin activity in both HS and LS rats. After inhibition of ACE with captopril, or of angiotensin II type I (AT1) receptor with losartan, the increase in RVR with L-NAME remained greater in HS than LS rats.(ABSTRACT TRUNCATED AT 250 WORDS)
由于饮食中盐分摄入增加会增强肾脏中一氧化氮（NO）的生成，我们研究了以下假说：盐摄入量的变化通过L-精氨酸-NO途径对肾脏血管阻力产生特定影响。我们对比了在麻醉大鼠静脉输注不同剂量的一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）期间，肾脏和后肢血管阻力（RVR和HQVR）的变化。将大鼠分为几组（每组n = 8至10只），分别给予高盐（HS）或低盐（LS）饮食两周。与LS组相比，HS组大鼠的平均动脉压升高幅度更大（ΔMAP；+32±4 vs. +22±3%；P = 0.05），RVR升高幅度更大（+160±17 vs. +83±10%；P < 0.005），肾血流量下降幅度更大（ΔRBF；-47±3 vs. -32±4%；P < 0.01）；两组的HQVR变化相似。HS组大鼠对L-NAME的RVR反应增强不能归因于更高肾灌注压（RPP），因为在通过调整肾上腹主动脉夹控制RPP的大鼠中这种增强仍然存在。HS组和LS组大鼠使用NO供体（SIN-1）时RVR变化相似。L-NAME降低了HS组和LS组大鼠的血浆肾素活性。用卡托普利抑制ACE或用氯沙坦抑制血管紧张素II 1型（AT1）受体后，HS组大鼠L-NAME引起的RVR升高仍大于LS组大鼠。（摘要截断于250字）
