Abstract
An elevated total peripheral resistance is the haemodynamic hallmark of both arterial hypertension and congestive heart failure. In essential hypertension it is the main pathogenetic abnormality, whereas in congestive heart failure it is the result of vasoconstriction serving to compensate for the fall in cardiac output and arterial pressure. Any drug that lowers total peripheral resistance can, therefore, potentially favourably influence established hypertension as well as unload the left ventricle in congestive failure. In essential hypertension, urapidil lowers arterial pressure acutely by a fall in total peripheral resistance with a small compensatory increase in cardiac output. Concomitantly, renal and splanchnic blood flow increase and the resistance in these vascular beds falls. In congestive heart failure, the acute administration of urapidil increases cardiac index and lowers mean pulmonary artery wedge pressure and systemic vascular resistance by about 30%. At the same time, a mild fall in mean arterial pressure is observed. Long term non-invasive studies document that these acute haemodynamic effects remain preserved in both arterial hypertension and congestive heart failure. Urapidil seems, therefore, to be a promising agent for the treatment of haemodynamic disorders that are characterised by an elevation of total peripheral resistance, such as established essential hypertension and congestive heart failure.