Grisk O, Frey B A, Uber A, Rettig R
Department of Physiology, Ernst-Moritz-Arndt-University, D-17487 Greifswald, Germany.
Am J Physiol Regul Integr Comp Physiol. 2000 Nov;279(5):R1737-44. doi: 10.1152/ajpregu.2000.279.5.R1737.
The contribution of elevated sympathetic activity to the development of renal posttransplantation hypertension was investigated. F1 hybrids (F1H) from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were transplanted with either an SHR or an F1H kidney and bilaterally nephrectomized. Three weeks after transplantation, sympathetic activity was assessed by measuring adrenal tyrosine hydroxylase (TH) mRNA content and recording splanchnic nerve activity (SNA) in conscious animals. To investigate the dependence of arterial pressure on sympathetic activity, animals were treated with the alpha(2)-adrenoceptor agonist guanabenz intracerebroventricularly. Mean arterial pressure (MAP) was 143 +/- 4 mmHg in recipients of an SHR kidney (n = 15) versus 110 +/- 3 mmHg in recipients of an F1H kidney (n = 10; P < 0.001). Adrenal TH mRNA content was 1.93 +/- 0.15 fmol/microg total RNA in recipients of an SHR kidney versus 1.96 +/- 0.17 fmol/microg total RNA in recipients of an F1H kidney (not significant). SNA did not differ significantly between recipients of an SHR kidney (n = 8) and recipients of an F1H kidney (n = 7) in terms of frequency and amplitude of synchronized nerve discharges. In response to cumulative intracerebroventricular administration of 10 and 20 microg guanabenz, SNA fell to 51 +/- 5% of control in recipients of an SHR kidney versus 44 +/- 6% of control in recipients of an F1H kidney (not significant) accompanied by a slight fall in MAP in either group. The results suggest that elevated sympathetic activity is not a major contributor to the development of renal posttransplantation hypertension.
研究了交感神经活动增强对肾移植后高血压发生发展的作用。将自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）的F1杂种（F1H）移植SHR或F1H肾脏，并进行双侧肾切除。移植后3周，通过测量清醒动物肾上腺酪氨酸羟化酶（TH）mRNA含量和记录内脏神经活动（SNA）来评估交感神经活动。为了研究动脉血压对交感神经活动的依赖性，给动物脑室内注射α（2）-肾上腺素能受体激动剂胍那苄。接受SHR肾脏的受体平均动脉压（MAP）为143±4 mmHg（n = 15），而接受F1H肾脏的受体为110±3 mmHg（n = 10；P < 0.001）。接受SHR肾脏的受体肾上腺TH mRNA含量为1.93±0.15 fmol/μg总RNA，接受F1H肾脏的受体为1.96±0.17 fmol/μg总RNA（无显著差异）。就同步神经放电的频率和幅度而言，接受SHR肾脏的受体（n = 8）和接受F1H肾脏的受体（n = 7）之间的SNA无显著差异。在累积脑室内注射10和20 μg胍那苄后，接受SHR肾脏的受体SNA降至对照的51±5%，接受F1H肾脏的受体降至对照的44±6%（无显著差异），两组MAP均略有下降。结果表明，交感神经活动增强不是肾移植后高血压发生发展的主要因素。
