The effects of a beta 1-blocking agent, atenolol, on blood pressure, plasma renin activity and prostaglandin F2 alpha excretion in patients with essential hypertension.

The antihypertensive action of beta-blocking agents has been suggested to be associated with the decrease in plasma renin activity (PRA) and can be antagonized by indomethacin, a prostaglandin (PG) synthesis inhibitor. We studied the acute and long-term effects of a beta 1-blocking agent, atenolol (50 mg b.i.d.), on blood pressure (BP), PRA and urinary PGF2 alpha excretion in 12 male patients (40 years old) with essential hypertension. BP was measured by means of a brachial cuff. PRA and PGF2 alpha were estimated radioimmunologically. One day after the initiation of atenolol treatment, BP fell significantly, the supine values from 159/114 to 143/104 mmHg and the erect from 158/118 to 140/106 mmHg. In six weeks BP decreased further to 135/94 and 134/96 mmHg, respectively. After the cessation of atenolol for three weeks BP rose to the pre-atenolol level. When the dose was readjusted (25-150 mg daily for 26 weeks), diastolic BP remained at 100 mmHg or higher in only two patients. During the atenolol treatment PRA declined to one-third of the pre-atenolol level in one day and to one-half in six weeks. The urinary excretion of PGF2 alpha was not affected by atenolol. Our results suggest that 1) the antihypertensive action of atenolol and the reduction of PRA are substantial already in one day, and 2) the decrease in BP or PRA is not associated with PGF2 alpha production.