Institute of Cardiovascular Physiology, Vascular Research Centre, Fachbereich Medizin, Goethe University, Frankfurt (Main), Germany.
Department of Nephrology & Diabetology, Carl-Thiem Hospital, Cottbus, Germany.
PLoS One. 2022 Mar 9;17(3):e0265086. doi: 10.1371/journal.pone.0265086. eCollection 2022.
Blood pressure is known to be increased in kidney donors following living-donor kidney transplantation. However, the physiological underpinnings of the blood-pressure increase following uninephrectomy remain unclear. We hypothesized that changes in sympathetic tone or in parasympathetic modulation of sinus node function are involved in the blood-pressure increase following experimental kidney-mass reduction.
C57BL6N mice (6 to 11 per group) subjected to sham surgery (controls) or uninephrectomy with or without a one-week course of sodium chloride-enriched, taurine-deficient diet were studied. Uninephrectomized mice treated with a subcutaneous infusion of angiotensin-II over a period of one week were positive controls. A transfemoral aortic catheter with telemetry unit was implanted, readings of heart-rate and blood-pressure were recorded. Powerspectral analysis of heart rate and systolic blood pressure was performed to gain surrogate parameters of sympathetictone and parasympathetic modulation of sinus node function. Baroreflex sensitivity of heart rate was determined from awake, unrestrained mice using spontaneous baroreflex gain technique.
Systolic arterial blood pressure, heart rate and baroreflex sensitivity were not different in uninephrectomized mice when compared to controls. Parasympathetic modulation of sinus node function was less in uninephrectomized mice in comparison to controls. Uninephrectomized mice of the high-angiotensin-II model or of the high-salt and taurine-deficiency model had an increased systolic arterial blood pressure.
Uninephrectomy associated with less parasympathetic modulation of sinus node function. The combination of uninephrectomy, taurine-deficiency and high-salt intake led to arterial hypertension.
已知在活体供肾移植后,肾供体的血压会升高。然而,单侧肾切除术后血压升高的生理基础尚不清楚。我们假设,交感神经张力或窦房结功能的副交感神经调制的变化参与了实验性肾质量减少后的血压升高。
对 6 至 11 只 C57BL6N 小鼠(每组 6 至 11 只)进行假手术(对照组)或单侧肾切除术,并进行为期一周的富含氯化钠、缺乏牛磺酸的饮食治疗。用皮下输注血管紧张素-II 治疗一周的单侧肾切除小鼠作为阳性对照。植入经股主动脉导管和遥测单元,记录心率和血压读数。进行心率和收缩压的功率谱分析,以获得交感神经张力和窦房结功能副交感神经调制的替代参数。使用自发血压反射增益技术从清醒、不受约束的小鼠中确定心率的血压反射敏感性。
与对照组相比,单侧肾切除小鼠的收缩压、心率和血压反射敏感性没有差异。与对照组相比,单侧肾切除小鼠的窦房结功能副交感神经调制减少。高血管紧张素-II 模型或高盐和牛磺酸缺乏模型的单侧肾切除小鼠的收缩压升高。
单侧肾切除与窦房结功能副交感神经调制减少有关。单侧肾切除、牛磺酸缺乏和高盐摄入的组合导致了动脉高血压。