CARDIOVASCULAR EFFECTS OF NOISE

  • 1 January 1982
    • journal article
    • research article
    • Vol. 657, 1-+
Abstract
The acute hemodynamic and hormonal effects induced by short-term exposure to loud noise were studied in men. Loud noise (95 or 100 dBA) increased blood pressure in healthy normotensive subjects and in patients with essential hypertension. The blood pressure elevation was caused by vasoconstriction in patients with essential hypertension and in normotensive subjects with a positive family history of hypertension, while the blood pressure response in normotensive subjects without a family history of hypertension was due mainly to an increase in cardiac output. This might indicate that there are genetically determined differences in the cardiovascular response to noise. Stimulation with noise did not increase plasma levels of catecholamines, prolactin, cortisol or growth hormone in normotensive subjects. In patients with essential hypertension, plasma noradrenaline [norepinephrine] increased, while plasma adrenaline [epinephrine] and plasma renin activity did not change. The increase in diastolic blood pressure caused by loud noise was not affected by .beta.1-selective or nonselective .beta.-adrenoceptor blockade or by .alpha.1- or combined .alpha.1- and nonselective .beta.-adrenoceptor blockade. The elevation in blood pressure induced by noise was usually mediated by vasoconstriction, i.e., an .alpha.1 effect. When .alpha.1-adrenoceptors were blocked, the blood pressure response to noise was mediated by an increase in cardiac output, i.e., a .beta.-adrenoceptor-mediated effect. An increased blood pressure was essential during exposure to loud noise. If part of the sympathetic nerve system was blocked, other parts could be activated in order to preserve the blood pressure at an elevated level. This indicated a temporary resetting of the baroreceptors during exposure to noise, which probably was mediated by the hypothalamus.