Ponchon P, Elghozi J L
Laboratoire de pharmacologie, CNRS URA 1482, faculté de médeine Necker-Enfants Malades, Paris.
Arch Mal Coeur Vaiss. 1995 Aug;88(8):1203-7.
Spectral analysis was recently chosen to characterize the fast oscillations depending on the autonomic nervous system. Humoral stimuli could impinge on low frequency (LF) domain of blood pressure (BP) since the time lag to humoral systems activation is larger. This study was designed to analyse LF components of short-term variability of BP of conscious rats in conditions where humoral systems were activated. We studied rats with two-kidney Goldblatt hypertension in which the BP level was dependent upon the renin-angiotensin and kallikrein-kinin systems. Spectral powers of the systolic and diastolic BP and heart rate (HR) were computed in the high (respiratory, HF), mid (0.2-0.6 Hz, MF) and low (0.02-0.2 Hz, LF) frequency bands, as detected by the Fast Fourier Transform technique on consecutive 102-s stationary periods. Renal hypertension by a two-kidney one clip procedure was associated with a marked rise in SBP (+47 mmHg) and no significant change in HR. Renal hypertension selectively increased the LF component of SBP (+86%) when hypertensive rats were compared to sham operated animals. First, administration of losartan, a selective nonpeptide angiotensin II receptor antagonist, to sham rats resulted in a moderate SBP decrease, a significant tachycardia (+47 batt/min) with no change in BP and HR spectra profiles. Losartan determined in the hypertensive group a marked fall in SBP (-25 mmHg) with a significant tachycardia (+50 batt/min). Interestingly, losartan reduced the LF component of SBP (-26%). In a second series of normotensive and hypertensive rats, Hoe 140, a bradykinin B-2 receptor antagonist, did not affect the BP and HR levels of the two groups of rats. Hoe 140 decreased the LF component of SBP variability (-28%). Losartan, added after Hoe 140, decreased the BP (-17 mmHg) in association with a tachycardia (+59 batt/min) and induced a supplementary decrease of the LF component of SBP variability (-60%) in hypertensive rats. After the combined blockade, the LF component of SBP of the hypertensive rats was equivalent to that of the sham rats. Thus, an increase in the LF component of BP variability was observed in a model of hypertension where the BP is dependent upon humoral factors. The contribution of the renin-angiotensin and kallikrein-kinin systems in the slow fluctuations of BP was demonstrated using two specific antagonists losartan and Hoe 140.
最近选择光谱分析来表征依赖自主神经系统的快速振荡。体液刺激可能会影响血压(BP)的低频(LF)域,因为体液系统激活的时间滞后较大。本研究旨在分析在体液系统激活的情况下清醒大鼠血压短期变异性的LF成分。我们研究了双肾Goldblatt高血压大鼠,其血压水平依赖于肾素-血管紧张素和激肽释放酶-激肽系统。通过快速傅里叶变换技术在连续102秒的平稳期检测收缩压和舒张压以及心率(HR)在高(呼吸,HF)、中(0.2-0.6Hz,MF)和低(0.02-0.2Hz,LF)频段的频谱功率。双肾单夹法所致肾性高血压与收缩压显著升高(+47mmHg)相关,而心率无显著变化。与假手术动物相比,肾性高血压选择性地增加了收缩压的LF成分(+86%)。首先,给假手术大鼠给予氯沙坦(一种选择性非肽类血管紧张素II受体拮抗剂)导致收缩压适度下降,显著心动过速(+47次/分钟),血压和心率频谱特征无变化。氯沙坦使高血压组收缩压显著下降(-25mmHg),伴有显著心动过速(+50次/分钟)。有趣的是,氯沙坦降低了收缩压的LF成分(-26%)。在第二组正常血压和高血压大鼠中,缓激肽B-2受体拮抗剂Hoe 140不影响两组大鼠的血压和心率水平。Hoe 140降低了收缩压变异性的LF成分(-28%)。在Hoe 140之后添加氯沙坦,使血压下降(-17mmHg),伴有心动过速(+59次/分钟),并导致高血压大鼠收缩压变异性的LF成分进一步降低(-60%)。联合阻断后,高血压大鼠收缩压的LF成分与假手术大鼠相当。因此,在血压依赖于体液因素的高血压模型中观察到血压变异性的LF成分增加。使用两种特异性拮抗剂氯沙坦和Hoe 140证明了肾素-血管紧张素和激肽释放酶-激肽系统在血压缓慢波动中的作用。