Lohmeier T E, Hildebrandt D A
University of Mississippi Medical Center, Department of Physiology and Biophysics, Jackson 39216-4505, USA.
Hypertension. 1998 Jan;31(1 Pt 2):429-34. doi: 10.1161/01.hyp.31.1.429.
To determine whether the sympathetic nervous system contributes to the hypertension induced by pathophysiological increments in plasma angiotensin II (Ang II) concentration, we determined the neurally induced changes in renal excretory function during chronic intravenous infusion of Ang II. Studies were carried out in five conscious chronically instrumented dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-hour urine collection from the denervated and innervated kidneys. After control measurements, Ang II was infused for 5 days at a rate of 4.8 pmol/kg per minute (5 ng/kg per minute); this was followed by a 5-day recovery period. Twenty-four-hour control values for mean arterial pressure (MAP) and for the ratio of denervated to innervated kidneys (DEN/INN) for urinary sodium, potassium, and creatinine excretion were 93+/-5 mm Hg, 1.17+/-0.09, 1.10+/-0.10, and 1.00+/-0.02, respectively. As expected, Ang II infusion caused sodium retention for several days before sodium balance was achieved at an elevated MAP (day 5=124+/-4 mm Hg). Moreover, by day 2 of Ang II-induced hypertension, there were significant reductions in the DEN/INN for sodium and potassium, which persisted for the 5 days of Ang II infusion; on day 5, the DEN/INN values for sodium and potassium were 0.71+/-0.10 and 0.91+/-0.12, respectively. In contrast, the DEN/INN for creatinine was unchanged from control levels during Ang II infusion, and measurements of renal hemodynamics indicated comparable reductions in glomerular filtration rate (approximately 13%) and renal plasma flow (approximately 25%) during Ang II infusion. This indicates that the renal nerves promoted sodium and potassium excretion during Ang II-induced hypertension by inhibiting tubular reabsorption of these electrolytes. Thus, this study provides no support for the hypothesis that increased renal sympathetic nerve activity impairs sodium excretion and contributes to Ang II-induced hypertension.
为了确定交感神经系统是否参与血浆血管紧张素II（Ang II）浓度的病理生理升高所诱导的高血压，我们在慢性静脉输注Ang II期间测定了神经诱导的肾排泄功能变化。研究在五只清醒的、长期植入仪器的犬身上进行，这些犬接受了单侧肾去神经支配，并将膀胱手术分为半膀胱，以便分别收集去神经支配侧和有神经支配侧肾脏的24小时尿液。在进行对照测量后，以每分钟4.8 pmol/kg（每分钟5 ng/kg）的速率输注Ang II 5天；随后是5天的恢复期。平均动脉压（MAP）以及去神经支配侧与有神经支配侧肾脏在尿钠、钾和肌酐排泄方面的比值（DEN/INN）的24小时对照值分别为93±5 mmHg、1.17±0.09、1.10±0.10和1.00±0.02。正如预期的那样，在升高的MAP（第5天 = 124±4 mmHg）达到钠平衡之前，输注Ang II导致钠潴留数天。此外，在Ang II诱导的高血压的第2天，钠和钾的DEN/INN显著降低，并在输注Ang II的5天内持续存在；在第5天，钠和钾的DEN/INN值分别为0.71±0.10和0.91±0.12。相比之下，在输注Ang II期间，肌酐的DEN/INN与对照水平相比没有变化，并且肾血流动力学测量表明在输注Ang II期间肾小球滤过率（约13%）和肾血浆流量（约25%）有类似程度的降低。这表明在Ang II诱导的高血压期间，肾神经通过抑制这些电解质的肾小管重吸收促进了钠和钾的排泄。因此，本研究不支持肾交感神经活动增加会损害钠排泄并导致Ang II诱导的高血压这一假说。
