Mechanism of antihypertensive effect of atenolol in patients with borderline hypertension during short-term treatment. A comprehensive study

Short-term treatment with 1-(p-carbamoyl-methylphenoxy)-3-isopropylamino)-2-propanol (atenolol, Tenormin®) (100 mg/d for 5 days) was conducted in 12 patients with labile essential hypertension. Before and at the end of the treatment, cardiohemodynamics, renal hemodynamic and excretory function, and renal pressur (renin-angiotensin-aldosterone) and depressor (renal kallikrein-kinin and prostaglandin) systems were examined. Atenolol decreased cardiac output (CO) without affecting total peripheral resistance. Atenolol also decreased plasma renin activity, plasma aldosterone concentration, urinary excretion of kallikrein-kinin, and urinary excretion of potassium whereas it increased plasma potassium concentration. Urinary excretion of prostaglandin E and sodium was not affected by atenolol. Glomerular filtration rate decreased, but renal plasma flow remained unchanged during the treatment by atenolol. A significant positive correlation was found between the changes in CO and in systolic blood pressure (SBP) while negative correlation was observed between the changes in total peripheral resistance and in SBP. A significant positive correlation was also noted between urinary kallikrein excretion and renal plasma flow. The change in urinary kinin excretion was conversely correlated to that in SBP. This study demonstrates that the hypotensive mechamism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothesized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.