Indenolol is a noncardioselective beta-adrenoceptor blocking drug with partial agonist activity. The mechanism of its acute antihypertensive activity has been evaluated in a double-blind, inpatient, crossover, randomized study versus placebo in 12 patients (eight men, four women, mean age 53 +/- 13 yr) with I and II WHO grade essential hypertension. Patients discontinued all antihypertensive and diuretic drugs at least 4 weeks before entry into the study. The effects of indenolol (120 mg) and placebo (2 weeks apart) were measured, in the same patient, 2 hours after a single oral administration. Variations of cardiac function were assessed by radionuclide angiocardiography, renal blood flow by sequential scintigraphy, and leg blood flow by strain-gauge plethysmography. Compared with placebo, indenolol reduced systolic blood pressure by 27.9 mm Hg and diastolic blood pressure by 17.1 mm Hg. Heart rate was also significantly decreased. The hemodynamic profile of indenolol activity was characterized by a decrease of cardiac index, without significant changes in systemic vascular resistance. Both renal and leg blood flow were increased by indenolol, and vascular resistance in these districts was considerably reduced. The percent reduction of renal vascular resistance was correlated significantly with the percent reduction of mean blood pressure. In conclusion, acute administration of indenolol exerts a considerable antihypertensive activity associated with a marked vasodilation in vascular districts involved in the progression of hypertensive disease such as the renal and muscular vasculature.
Renal and limb vasodilatation during acute beta-adrenoceptor blockade with indenolol.
BISI, Gianni;
1995-01-01
Abstract
Indenolol is a noncardioselective beta-adrenoceptor blocking drug with partial agonist activity. The mechanism of its acute antihypertensive activity has been evaluated in a double-blind, inpatient, crossover, randomized study versus placebo in 12 patients (eight men, four women, mean age 53 +/- 13 yr) with I and II WHO grade essential hypertension. Patients discontinued all antihypertensive and diuretic drugs at least 4 weeks before entry into the study. The effects of indenolol (120 mg) and placebo (2 weeks apart) were measured, in the same patient, 2 hours after a single oral administration. Variations of cardiac function were assessed by radionuclide angiocardiography, renal blood flow by sequential scintigraphy, and leg blood flow by strain-gauge plethysmography. Compared with placebo, indenolol reduced systolic blood pressure by 27.9 mm Hg and diastolic blood pressure by 17.1 mm Hg. Heart rate was also significantly decreased. The hemodynamic profile of indenolol activity was characterized by a decrease of cardiac index, without significant changes in systemic vascular resistance. Both renal and leg blood flow were increased by indenolol, and vascular resistance in these districts was considerably reduced. The percent reduction of renal vascular resistance was correlated significantly with the percent reduction of mean blood pressure. In conclusion, acute administration of indenolol exerts a considerable antihypertensive activity associated with a marked vasodilation in vascular districts involved in the progression of hypertensive disease such as the renal and muscular vasculature.
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