Moyses M R, Cabral A M, Bissoli N, Vasquez E C
Department of Physiological Sciences, Biomedical Center, UFES, Vitoria, Brazil.
Hypertension. 1994 Jan;23(1 Suppl):I87-92. doi: 10.1161/01.hyp.23.1_suppl.i87.
The present study examined the time course of changes in baroreceptor reflex function by means of sigmoidal curve-fitting analysis in conscious, unrestrained renovascular one-kidney, one clip (1K1C) rats at 1, 3, 7, 15, 30, and 60 days after renal artery clipping. The reflex heart rate responses were elicited by alternate intravenous bolus injections of phenylephrine (change, +5 to +50 mm Hg) and sodium nitroprusside (change, -5 to -50 mmHg). Atropine methylnitrate and atenolol were given to evaluate the responses mediated by the cardiac sympathetic or vagal component, respectively. The average baroreceptor reflex gain (sensitivity) decreased progressively (day 1, 3.35 +/- 0.3 beats per minute [bpm] per millimeter of mercury), reaching a maximal attenuation in the 30-day 1K1C group (1.83 +/- 0.5 bpm/mm Hg) compared with sham rats (approximately 4.60 bpm/mm Hg). The data showed a decreased vagal activity contributing to the attenuation of the baroreceptor gain only in the 30-day 1K1C group. In contrast, the cardiac sympathetic component of the baroreceptor reflex was significantly decreased in all 1K1C groups (from 2.10 +/- 0.4 to 0.50 +/- 0.2 bpm/mm Hg) compared with the respective sham groups (from 3.80 +/- 0.3 to 3.10 +/- 0.4 bpm/mm Hg). These results suggest that a reduced contribution of the sympathetic component to the baroreceptor heart rate reflex may be the main cause of the progressive attenuation of the baroreceptor reflex sensitivity observed in conscious 1K1C hypertensive rats.
本研究通过S形曲线拟合分析,检测了清醒、未束缚的肾血管性单肾单夹(1K1C)大鼠在肾动脉夹闭后1天、3天、7天、15天、30天和60天压力感受器反射功能变化的时间进程。通过交替静脉推注去氧肾上腺素(变化范围为+5至+50 mmHg)和硝普钠(变化范围为-5至-50 mmHg)来引发反射性心率反应。分别给予硝酸甲基阿托品和阿替洛尔,以评估由心脏交感神经或迷走神经成分介导的反应。压力感受器反射增益(敏感性)平均逐渐降低(第1天,3.35±0.3次/分钟[bpm]/毫米汞柱),与假手术大鼠(约4.60 bpm/毫米汞柱)相比,在30天的1K1C组中达到最大衰减(1.83±0.5 bpm/毫米汞柱)。数据显示,仅在30天的1K1C组中,迷走神经活动降低导致压力感受器增益衰减。相比之下,与各自的假手术组(从3.80±0.3至3.10±0.4 bpm/毫米汞柱)相比,所有1K1C组的压力感受器反射的心脏交感神经成分均显著降低(从2.10±0.4至0.50±0.2 bpm/毫米汞柱)。这些结果表明,交感神经成分对压力感受器心率反射的贡献降低可能是清醒1K1C高血压大鼠中观察到的压力感受器反射敏感性逐渐衰减的主要原因。