Burke S L, Malpas S C, Head G A
Neuropharmacology Laboratory, Baker Medical Research Institute, Melbourne, Victoria, Australia.
J Auton Nerv Syst. 1998 Oct 15;72(2-3):177-86. doi: 10.1016/s0165-1838(98)00103-9.
Environmental stress can cause an increase in sympathetic nerve activity both in humans and animals. While centrally acting antihypertensive drugs such as rilmenidine are known to reduce sympathetic tone, it is not clear whether they also influence the cardiovascular responses to acute stress. In the present study we examined the effects of systemic treatment with rilmenidine on the sympathetic and haemodynamic responses to air jet or noise stress. Twelve conscious rabbits previously implanted with a renal nerve recording electrode were subjected to an 8 l/min stream of air directed at their face for 10 min or exposure to 10 min of white noise (approximately 85 dB). Both air jet and noise stress elicited increases in renal sympathetic nerve activity (RSNA) which were greatest in the first minute (+55+/-9% and +40+/-6%, respectively), but which quickly reached a stable level over the subsequent 9 min (+24+/-6% and +9+/-5%, respectively). This was accompanied by a small increase in heart rate (HR) and mean arterial pressure (MAP). Intravenous rilmenidine (273 microg/kg) reduced MAP from 85+/-3 mm Hg to 68+/-2 mm Hg and HR from 203+/-10 b/min to 188+/-10 b/min and lowered basal RSNA by 54%. Rilmenidine reduced the increase in RSNA seen during the first minute of air jet stress by 35% and reduced the average increase over the next 9 min by 68%. However, rilmenidine had little effect on either the initial or stable RSNA responses to noise stress. Saline treatment did not alter the RSNA responses to either air jet or noise stress. The results show that centrally-acting antihypertensive agents not only lower basal RSNA, but can differentially influence environmentally induced sympathetic responses. In addition, the differential effect of rilmenidine on noise and air jet stress suggests that they may involve quite different central processing.
环境应激可导致人和动物交感神经活动增加。虽然已知如利美尼定等中枢性抗高血压药物可降低交感神经张力，但它们是否也会影响对急性应激的心血管反应尚不清楚。在本研究中，我们检测了利美尼定全身给药对空气喷射或噪声应激引起的交感神经和血流动力学反应的影响。将12只预先植入肾神经记录电极的清醒家兔，面部接受8升/分钟的气流吹拂10分钟，或暴露于10分钟的白噪声（约85分贝）中。空气喷射和噪声应激均引起肾交感神经活动（RSNA）增加，在第一分钟增加最为明显（分别为+55±9%和+40±6%），但在随后的9分钟内迅速达到稳定水平（分别为+24±6%和+9±5%）。同时伴有心率（HR）和平均动脉压（MAP）小幅升高。静脉注射利美尼定（273微克/千克）使MAP从85±3毫米汞柱降至68±2毫米汞柱，HR从203±10次/分钟降至188±10次/分钟，并使基础RSNA降低54%。利美尼定使空气喷射应激第一分钟内RSNA的增加减少35%，并使接下来9分钟内的平均增加减少68%。然而，利美尼定对噪声应激初始或稳定的RSNA反应几乎没有影响。生理盐水处理未改变对空气喷射或噪声应激的RSNA反应。结果表明，中枢性抗高血压药物不仅降低基础RSNA，而且可不同程度地影响环境诱导的交感反应。此外，利美尼定对噪声和空气喷射应激的不同作用表明，它们可能涉及截然不同的中枢处理过程。
