Effect of rilmenidine on the cadiovascular responses to stress in the conscious rabbit.

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.