Schneider K, Gross V, Lippoldt A, Luft F C
Franz Volhard Clinic, Berlin, Germany.
J Hypertens. 1997 Sep;15(9):1041-8. doi: 10.1097/00004872-199715090-00016.
Hypertension features an exaggerated natriuresis after acute volume expansion. In humans, the degree of exaggerated natriuresis appears to be correlated inversely to the level of angiotensin (Ang) II.
To test the hypothesis that the degree of exaggerated natruresis is correlated to the level of Ang II by studying two rat models, transgenic rats (TGR) with and extra renin gene (TGR mRen2)27 and desoxycorticosterone acetate (DOCA)-salt rats, in comparison with Sprague-Dawley Hannover (SDH) rat controls.
All of the rats were uninephrectomized for 1 month. DOCA-salt rats were implanted with a DOCA pallet and drank 1% saline. Rats were anesthetized and their left kidneys were instrumented with renal sympathetic nerve activity (RSNA) electrodes and laser-Doppler cortical and medullary flow probes. The glomerular filtration rate, diuresis, and natriuresis were measured for 120 min after sodium loading (5% body weight 0.9% saline administered during 3 min). Kidneys were examined histologically.
The blood pressure in TGR and DOCA-salt rats was 40-50 mmHg higher than that in SDH rats, and decreased briefly after volume expansion for all groups. The diuresis and natriuresis of TGR and DOCA-salt rats were greater than those of SDH rats. The medullary blood flow increased and the cortical blood flow in SDH decreased, whereas the cortical blood flow in TGR and DOCA-salt rats remained high. The RSNA in rats of all groups decreased; however, this decrease was greater in SDH than it was in TGR and DOCA-salt rats. The histology was affected most severely for the DOCA-salt rats.
Exaggerated natriuresis occurred in hypertensive rats regardless of their Ang II status. Both strains were characterized by a smaller decrease in RSNA and a preserved cortical blood flow in the face of volume expansion. These data do not support the notion that exaggerated natriuresis is a function of renin-level suppression for rats.
高血压的特征是急性容量扩张后出现过度利钠。在人类中，过度利钠的程度似乎与血管紧张素（Ang）II的水平呈负相关。
通过研究两种大鼠模型，即携带额外肾素基因的转基因大鼠（TGR）（TGR mRen2）27和醋酸去氧皮质酮（DOCA）-盐大鼠，并与斯普拉格-道利汉诺威（SDH）大鼠对照，来检验过度利钠程度与Ang II水平相关的假说。
所有大鼠均进行单侧肾切除1个月。DOCA-盐大鼠植入DOCA药托并饮用1%盐水。大鼠麻醉后，其左肾安装肾交感神经活动（RSNA）电极以及激光多普勒皮质和髓质血流探头。在钠负荷（3分钟内给予5%体重的0.9%盐水）后120分钟测量肾小球滤过率、尿量和尿钠排泄量。对肾脏进行组织学检查。
TGR和DOCA-盐大鼠的血压比SDH大鼠高40 - 50 mmHg，所有组在容量扩张后血压均短暂下降。TGR和DOCA-盐大鼠的利尿和利钠作用大于SDH大鼠。SDH大鼠的髓质血流增加而皮质血流减少，而TGR和DOCA-盐大鼠的皮质血流保持较高水平。所有组大鼠的RSNA均下降；然而，SDH大鼠的下降幅度大于TGR和DOCA-盐大鼠。DOCA-盐大鼠的组织学受影响最严重。
高血压大鼠无论其Ang II状态如何都会出现过度利钠。两种品系的特征都是在容量扩张时RSNA下降较小且皮质血流得以保留。这些数据不支持过度利钠是大鼠肾素水平抑制作用的一种表现这一观点。
