Sivritas Sema-Hayriye, Ploth David W, Fitzgibbon Wayne R
Department of Medicine, Division of Nephrology, Medical University of South Carolina, 96 Jonathan Lucas Street, Charleston, SC 29425, USA.
Am J Physiol Renal Physiol. 2008 Sep;295(3):F811-7. doi: 10.1152/ajprenal.90225.2008. Epub 2008 Jul 16.
The present study was performed to test the hypothesis that under normal physiological conditions and/or during augmentation of kinin levels, intrarenal kinins act on medullary bradykinin B(2) (BKB(2)) receptors to acutely increase papillary blood flow (PBF) and therefore Na(+) excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB(2) receptor blockade on renal hemodynamics and excretory function in rats fed either a normal (0.23%)- or a low (0.08%)-NaCl diet. For each NaCl diet, two groups of rats were studied. Baseline renal hemodynamic and excretory function were determined during IMI infusion of 0.9% NaCl into the left kidney. The infusion was then either changed to HOE-140 (100 microg.kg(-1).h(-1), treated group) or maintained with 0.9% NaCl (time control group), and the parameters were again determined. In rats fed a normal-salt diet, HOE-140 infusion decreased left kidney Na(+) excretion (urinary Na(+) extraction rate) and fractional Na(+) excretion by 40 +/- 5% and 40 +/- 4%, respectively (P < 0.01), but did not alter glomerular filtration rate, inner medullary blood flow (PBF), or cortical blood flow. In rats fed a low-salt diet, HOE-140 infusion did not alter renal regional hemodynamics or excretory function. We conclude that in rats fed a normal-salt diet, kinins act tonically via medullary BKB(2) receptors to increase Na(+) excretion independent of changes in inner medullary blood flow.
在正常生理条件下和/或激肽水平升高时，肾内激肽作用于髓质缓激肽B2（BKB2）受体，从而急性增加乳头血流（PBF），进而增加钠排泄。我们测定了急性肾内髓质间质（IMI）BKB2受体阻断对喂食正常（0.23%）或低（0.08%）氯化钠饮食大鼠的肾血流动力学和排泄功能的影响。对于每种氯化钠饮食，研究了两组大鼠。在向左肾IMI输注0.9%氯化钠期间测定基线肾血流动力学和排泄功能。然后将输注液改为HOE-140（100μg·kg-1·h-1，治疗组）或维持0.9%氯化钠输注（时间对照组），并再次测定各项参数。在喂食正常盐饮食的大鼠中，输注HOE-140使左肾钠排泄（尿钠提取率）和钠排泄分数分别降低40±5%和40±4%（P<0.01），但不改变肾小球滤过率、肾内髓质血流（PBF）或皮质血流。在喂食低盐饮食的大鼠中，输注HOE-140不改变肾局部血流动力学或排泄功能。我们得出结论，在喂食正常盐饮食的大鼠中，激肽通过髓质BKB2受体持续发挥作用，增加钠排泄，且与肾内髓质血流变化无关。
