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Acute haemodynamic and humoral responses to felodipine and metoprolol in mild hypertension
Authors:R. Fagard  P. Lijnen  E. Moerman  J. Staessen  A. Amery
Affiliation:(1) Hypertension and Cardiovascular Rehabilitation Unit, Department of Pathophysiology, University of Leuven, Leuven, Belgium;(2) Heymans Institute of Pharmacology, University of Gent, Gent, Belgium;(3) Laboratorium voor Hartfunctie Inwendige Zieken-Cardiologie, UZ Pellenberg, Weligerveld 1, B-3041 Pellenberg, Belgium
Abstract:Summary Oral administration of felodipine to 10 patients with mild essential hypertension acutely reduced systemic vascular resistance (SVR) by 40% after 30 min. The change in SVR was significantly related to age (r=–0.74). The reduction in the intraarterially measured brachial artery pressure was limited to 15/13 mmHg, due to a rise in cardiac output (CO). The tachycardia was sustained for 90 min, as was an elevation of plasma noradrenaline. There was a transient increase in stroke volume, associated with a reduction in pulmonary capillary wedge pressure, which was at least partly due to a reduced intravascular volume. In contrast to SVR, pulmonary vascular resistance was not affected by felodipine. Addition of intravascular metoprolol after 90 min decreased HR and CO and augmented SVR. The felodipine-induced rise in plasma renin activity (PRA) of 100% was completely reversed by metoprolol. Plasma angiotensin II (PA II) rose by 15% during felodipine, whereas plasma aldosterone concentration (PAC) was not affected. Thus, actuely administered felodipine was a potent dilator of systemic but not of pulmonary arterioles, it stimulated the sympathetic nervous system, and reduced left ventricular filling pressure. The rise in plasma renin did not result in a higher plasma aldosterone level, due partly to reduced generation of angiotensin II.
Keywords:felodipine  metoprolol  hypertension  aldosterone  angiotensin  cardiac output  catecholamines  pulmonary vascular resistance  renin  systemic vascular resistance  haemodynamic effects
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