Ye S, Ozgur B, Campese V M
Department of Medicine, University of Southern California, Los Angeles, USA.
Kidney Int. 1997 Mar;51(3):722-7. doi: 10.1038/ki.1997.103.
Hypertension in 5/6 nephrectomized (CRF) rats is partly related to increased activity of the sympathetic nervous system. We have previously shown a greater norepinephrine turnover rate in the posterior hypothalamic nuclei and locus coeruleus of CRF than control rats. Dorsal rhizotomy prevented the rise in blood pressure and the increase in NE turnover rate in the posterior hypothalamus and the locus coeruleus. The studies suggest that afferent impulses from the kidney to central integrative structures in the brain may be responsible for hypertension in CRF rats. To further evaluate the role of renal afferent nerves in the regulation of blood pressure, and whether renal afferent pathways integrate with the posterior hypothalamus, we studied the effects of an intrarenal injection of 50 microliters of 10% phenol on blood pressure and NE secretion from the posterior hypothalamus of Sprague-Dawley rats. Mean arterial pressure increased from 89 +/- 4.0 to 114 +/- 4.3 mm Hg in rats which received intrarenal injection of phenol, but it did not change in rats that received vehicle (95 +/- 4.3 and 89 +/- 3.6 mm Hg, respectively). Renal denervation totally prevented the increase in blood pressure caused by intrarenal injection of phenol. The secretion of NE from the posterior hypothalamus increased from 139 +/- 4.8 to 250 +/- 9.9 pg/ml (P < 0.01) in rats that received intrarenal phenol, but it did not change in rats which received vehicle or in those with renal denervation. In CRF rats NE secretion from the posterior hypothalamus was greater than in control and CRF rats subjected to dorsal rhizotomy. These studies show that afferent impulses from an injured kidney increase NE secretion from the posterior hypothalamus and raise blood pressure. NE secretion is higher in the posterior hypothalamus of CRF than control rats. The posterior hypothalamus appears to be an important integrative structure of the sympathetic regulation of blood pressure.
5/6肾切除（慢性肾衰竭）大鼠的高血压部分与交感神经系统活性增加有关。我们之前已表明，与对照大鼠相比，慢性肾衰竭大鼠下丘脑后核和蓝斑中的去甲肾上腺素周转率更高。背根切断术可防止后下丘脑和蓝斑中血压升高以及去甲肾上腺素周转率增加。这些研究表明，从肾脏到大脑中枢整合结构的传入冲动可能是慢性肾衰竭大鼠高血压的原因。为了进一步评估肾传入神经在血压调节中的作用，以及肾传入通路是否与下丘脑后区整合，我们研究了向Sprague-Dawley大鼠肾内注射50微升10%苯酚对血压和下丘脑后区去甲肾上腺素分泌的影响。接受肾内注射苯酚的大鼠平均动脉压从89±4.0毫米汞柱升至114±4.3毫米汞柱，但接受赋形剂的大鼠平均动脉压未发生变化（分别为95±4.3和89±3.6毫米汞柱）。肾去神经支配完全阻止了肾内注射苯酚引起的血压升高。接受肾内苯酚注射的大鼠下丘脑后区去甲肾上腺素分泌从139±4.8皮克/毫升增至250±9.9皮克/毫升（P<0.01），但接受赋形剂的大鼠或肾去神经支配的大鼠去甲肾上腺素分泌未发生变化。在慢性肾衰竭大鼠中，下丘脑后区去甲肾上腺素分泌高于对照大鼠以及接受背根切断术的慢性肾衰竭大鼠。这些研究表明，来自受损肾脏的传入冲动会增加下丘脑后区去甲肾上腺素分泌并升高血压。慢性肾衰竭大鼠下丘脑后区的去甲肾上腺素分泌高于对照大鼠。下丘脑后区似乎是交感神经调节血压的重要整合结构。
