Hemodynamic Effects of Loud Noise before and after Central Sympathetic Nervous Stimulation

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Abstract
The hemodynamic effects of loud noise after central .alpha.2-adrenoceptor stimulation were studied in 13 patients with mild (WHO 1) essential hypertension. The patients were randomized (double-blind) to treatment with either placebo or guanfacine 1-2 mg for four weeks and then crossed over and treated for another four weeks. All patients were exposed to a loud broad-band noise (105 dBA fro 30 min) and all were studied both on placebo and guanfacine. Guanfacine significantly reduced the resting blood pressure from 141/92 to 134/88 mmHg (p < 0.01) as well as heart rate at rest from 63 to 58 beats/min (p < 0.05). Noise stimulation caused a significant increase in blood pressure and resistance in the placebo-treated group, while cardiac output decreased significantly. Pretreatment for one month with the central .alpha.2-adrenoceptor stimulating agent guanfacine did not block the noise-induced pressor response nor the increase in peripheral resistance. A significant decrease in stroke volume was observed and cardiac output also tended to decrease in this group. It could be concluded that loud noise is a potent pressor stimulus which causes vasoconstriction and that the blood pressure response during noise could not be blocked by the centrally acting antihypertensive agent guanfacine. Since noise causes vasoconstriction it also induces an increased tone in the small arteries and, if the noise stimulus is sufficiently strong and repeated for a long time, it might cause structural changes in the resistance vessels and permanent arterial hypertension in humans.