Hemodynamic effects of felodipine in hypertension: a review

Abstract

Felodipine is a new calcium antagonist that was developed aiming particularly at reduction in vascular resistance-without any decrease in heart pump function. Studies in animals have demonstrated that felodipine given intravenously induces an acute fall in total peripheral resistance and blood pressure (BP), associated with acute reflex tachycardia and an increase in cardiac output (CO). During chronic treatment, the reflex tachycardia is abolished, while resistance and BP remain reduced. Acute vasodilatation has been demonstrated in the heart, kidneys, intestines, and skeletal muscles. Increased blood flow has also been demonstrated in the coronary arteries. Acute studies in humans with essential hypertension have demonstrated similar effects to what has been observed in the spontaneously hypertensive rat (SHR): a marked fall in total peripheral resistance and BP-associated with reflex tachycardia and increased CO. There is also an increase in coronary renal, and forearm blood flow. Catheterization studies have indicated that felodipine also dilates large coronary arteries. During chronic treatment in 16 males with initial diastolic BP of 100-120 mm Hg, felodipine reduced total peripheral resistance approximately 15% at rest and during exercise without significant changes in cardiac index (CI), heart rate (HR), and stroke volume (SV). As in animals, no reflex tachycardia is seen during chronic treatment. It is concluded that felodipine reduces BP in hypertensive animals and humans because of the marked effect on total peripheral resistance. CO is not reduced either at rest or during exercise. During chronic treatment, reflex tachycardia is abolished.