TGF and nitric oxide: effects of salt intake and salt-sensitive hypertension.

TGF and nitric oxide: effects of salt intake and salt-sensitive hypertension.
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发表时间:
1996-06
期刊:
Kidney international. Supplement
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通讯作者:
Christopher S. Wilcox;Welch Wj
Christopher S. Wilcox;Welch Wj
中科院分区:
其他
文献类型:
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作者:
Christopher S. Wilcox;Welch Wj

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肾小管-肾小球反馈反应(TGF)导致致密斑(MD)段在NaCl重吸收期间传入小动脉(AA)的血管收缩以及肾小球毛细血管压(PGC)和单个肾单位肾小球滤过率(SNGFR)的下降。最近的研究得出的结论是,一氧化氮(NO)是由MD合成的,并减弱了TGF的反应。由于高盐(HS)饮食已被发现钝化TGF,我们测试了盐的摄入量对一氧化氮合成阻断反应的影响。对于第一个系列,从近端停流压(PSF)的变化评估TGF,PSF是PGC对Henle环(LH)分级灌注的反应指数,其中包括肾小管液(NTF)。用10(-3)M L-NMA环灌注不影响低盐(LS)大鼠的PSF反应,但在20 nl. ml-1(-1.5 +/- 0.4 mm Hg; P < 0.01)和40 nl.ml-1(-2.2 +/- 0.5 mm Hg; P < 0.001)灌注期间降低HS大鼠的PSF(P <0.01)。对于第二系列,将盐敏感性Dahl/Rapp(ssDR)大鼠的TGF应答与Sprague-Dawley(SD)大鼠进行比较。在开始HS或LS饮食后8至10天,通过以40 nl.min-1循环灌注人工肾小管液对两组进行研究。与Sprague-Dawley大鼠相比,ssDR在LS期间具有钝化的最大TGF应答(SD,8.2 +/- 0.3 vs. ssDR,6.4 +/- 0.3 mm Hg; P < 0.001),但在HS期间没有。在LS摄入期间,将L-NMA加入到灌注Henle袢的ATF中并没有改变任一菌株的最大TGF反应。然而,在HS摄入期间,L-NMA增加了SD大鼠的最大TGF反应(4.4 +/- 0.4至6.7 +/- 0.5 mm Hg; P < 0.001),但没有显著改变ssDR大鼠的PSF(5.2 +/- 0.3至5.7 +/- 0.5 mm Hg; NS)。我们的结论是,TGF的反应增强了NOS的封锁在HS,但不是LS摄入量;这种响应NOS封锁在HS摄入量在盐敏感的Dahl/Rapp大鼠丢失。
The tubuloglomerular feedback response (TGF) entails vasoconstriction of the afferent arteriole (AA) and a fall in the glomerular capillary pressure (PGC) and single nephron glomerular filtration rate (SNGFR) during NaCl reabsorption in the macula densa (MD) segment. Recent studies have concluded that nitric oxide (NO) is synthesized by the MD and blunts the TGF response. Since a high salt (HS) diet has been found to blunt TGF, we tested the effects of salt intake on the response to blockade of nitric oxide synthesis. For the first series, the TGF was assessed from changes in proximal stop-flow pressure (PSF, an index of PGC in response to graded perfusion of the loop of Henle (LH) with name tubular fluid (NTF). Loop perfusion with 10(-3) M L-NMA did not affect the PSF responses of low salt (LS) rats, but reduced (P < 0.01) the PSF of HS rats during perfusion at 20 nl.min-1 (-1.5 +/- 0.4 mm Hg; P < 0.01) and at 40 nl.ml-1 (-2.2 +/- 0.5 mm Hg; P < 0.001). For the second series, the TGF responses of salt sensitive Dahl/Rapp (ssDR) rats were compared to Sprague-Dawley (SD) rats. Both groups were studied 8 to 10 days after starting HS or LS diets by loop perfusion of artificial tubular fluid at 40 nl.min-1. Compared to Sprague-Dawley rats, the ssDR had blunted maximal TGF responses during LS (SD, 8.2 +/- 0.3 vs. ssDR, 6.4 +/- 0.3 mm Hg; P < 0.001), but not during HS. During LS intake, addition of L-NMA to ATF perfusing the loop of Henle did not alter the maximal TGF response of either strain. However, during HS intake L-NMA increased the maximal TGF response of SD rats (4.4 +/- 0.4 to 6.7 +/- 0.5 mm Hg; P < 0.001) but did not significantly change the PSF of ssDR rats (5.2 +/- 0.3 to 5.7 +/- 0.5 mm Hg; NS). We conclude that the TGF response is enhanced by blockade of NOS during HS, but not LS intakes; this response to NOS blockade during HS intake is lost in salt sensitive Dahl/Rapp rats.