ROLE OF NITRIC-OXIDE ON PAPILLARY BLOOD-FLOW AND PRESSURE NATRIURESIS
ROLE OF NITRIC-OXIDE ON PAPILLARY BLOOD-FLOW AND PRESSURE NATRIURESIS
复制标题
DOI：
10.1161/01.hyp.25.3.408
复制
发表时间：
1995-03-01
期刊：
影响因子：
8.3
通讯作者：
GARCIASALOM, M
中科院分区：
文献类型：
--
作者：
FENOY, FJ;FERRER, P;GARCIASALOM, M
本研究考察了一氧化氮合成阻断或增强（分别使用n -omega-硝基- l -精氨酸甲酯[L-NAME]或n -乙酰半胱氨酸）是否可以改变钠排泄、乳头状血流量和肾灌注压之间的关系。采用激光多普勒血流仪测量乳头状血流量。低剂量L-NAME （3.7 nmol/kg /分钟）仅在高动脉压（140 mm Hg）时减少乳头血流量，但对压力性尿钠无影响。在所有研究的灌注压力下，每分钟输注37 nmol/kg的L-NAME可使皮质血流量减少9%，在120和140 mm Hg下分别使乳头状血流量降低8%和19%，并减弱压力-钠尿反应。在动脉压100 ~ 140 mm Hg范围内，185 nmol/kg /分钟的L-NAME可使皮质血流量减少30%，使乳头血流量减少25%。所有剂量的L-NAME阻断一氧化氮合成研究表明，只有在高肾灌注压下，乳头状血流量才会减少，但在低灌注压下，乳头状血流量基本保持不变，从而恢复了乳头状血流量的自动调节。n -乙酰半胱氨酸（1.8 mmol/kg）使乳头血流量增加9%，改变了乳头血流量、钠排泄和肾灌注压之间的关系。n -乙酰半胱氨酸对乳头状血流量的影响被随后的L-NAME给药阻断。结果提示，随着肾灌注压升高，肾髓质一氧化氮水平升高可能是肾髓质血流自我调节缺失和容量扩张大鼠压力利钠反应的原因。
This study examined whether nitric oxide synthesis blockade or potentiation (with N-omega-nitro-L-arginine methyl ester [L-NAME] or N-acetylcysteine, respectively) can shift the relations between sodium excretion, papillary blood flow, and renal perfusion pressure. Papillary blood flow was measured by laser Doppler flowmetry. A low dose of L-NAME (3.7 nmol/kg per minute) reduced papillary blood flow only at high arterial pressure (140 mm Hg), but it had no effect on pressure natriuresis. Infusion of 37 nmol/kg per minute L-NAME reduced cortical blood flow by 9% at all perfusion pressures studied, lowered papillary blood how by 8% and 19% at 120 and 140 mm Hg, respectively, and blunted the pressure-natriuresis response. The administration of 185 nmol/kg per minute L-NAME reduced cortical blood flow by 30% and decreased papillary blood flow by 25% in the range of 100 to 140 mm Hg of arterial pressure. Blockade of nitric oxide synthesis with L-NAME at all doses studied reduced papillary blood flow only at high renal perfusion pressures, but papillary blood flow remained essentially unchanged at low perfusion pressures, thus restoring papillary blood flow autoregulation. N-Acetyl-cysteine (1.8 mmol/kg) increased papillary blood how by 9% and shifted the relations between papillary blood flow, sodium excretion, and renal perfusion pressure toward lower pressures. This effect of N-acetylcysteine on papillary blood flow was blocked by subsequent L-NAME administration. The results indicate that increases in renal medullary levels of nitric oxide as renal perfusion pressure rises may be responsible for the lack of renal medullary blood flow autoregulation and the pressure natriuretic response in volume-expanded rats.