Thirteen patients with mild essential hypertension, mean age 44 years (range 21–59), were studied during “stress” before and after postsynaptic α‐adrenoceptor blockade and combined postsynaptic α‐ and non‐selective β‐adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p<0.05), diastolic (9%, p<0.01) and mean arterial pressure (6%, p<0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p<0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic α‐adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p<0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic α‐ and non‐selective β‐adrenoceptor blockade (la‐be talol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p<0.01). Labetalol effectively blocked the stress‐induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined α‐ and β‐adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p<0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during “stress” but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.