[Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension: the effect of atenolol (author's transl)].
Plasmin noradrenaline concentration after bicycle exercise (200 W for 2 min), compared with base line concentration, was used as an index of sympathetic responsiveness in patients with essential hypertension. Atenolol (JCI 66082, a "cardioselective" beta-blocker) was given in a daily dose of 200 mg to 16 patients for five weeks. This caused a decrease in supine blood pressure of 37/23 and, on standing, of 36/25 mm Hg compared with the placebo period. There was a significant correlation between the ratio of the increase in plasma noradrenaline concentration on exercise over its base line concentration and the subsequent fall in mean arterial pressure (r=0.840; P less than 0.001). There was a less significant correlation between plasma renin concentration and subsequent decrease in mean arterial pressure (r=0.542; P less than 0.05). Administrations of atenolol caused a rise in plasma noradrenaline both on lying and after exercise (P less than 0.0125), and a fall in plasma renin concentration (P less than 0.01). The results suggest that the antihypertensive effect of atenolol is related to the responsiveness of the sympathetic nervous sytem. Adrenergic activity is apparently an important determinant of blood pressure response to beta-blockade.
[Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension: the effect of atenolol (author's transl)]. Plasmin noradrenaline concentration after bicycle exercise (200 W for 2 min), compared with base line concentration, was used as an index of sympathetic responsiveness in patients with essential hypertension. Atenolol (JCI 66082, a "cardioselective" beta-blocker) was given in a daily dose of 200 mg to 16 patients for five weeks. This caused a decrease in supine blood pressure of 37/23 and, on standing, of 36/25 mm Hg compared with the placebo period. There was a significant correlation between the ratio of the increase in plasma noradrenaline concentration on exercise over its base line concentration and the subsequent fall in mean arterial pressure (r=0.840; P less than 0.001). There was a less significant correlation between plasma renin concentration and subsequent decrease in mean arterial pressure (r=0.542; P less than 0.05). Administrations of atenolol caused a rise in plasma noradrenaline both on lying and after exercise (P less than 0.0125), and a fall in plasma renin concentration (P less than 0.01). The results suggest that the antihypertensive effect of atenolol is related to the responsiveness of the sympathetic nervous sytem. Adrenergic activity is apparently an important determinant of blood pressure response to beta-blockade.