Pleiotropic actions of cardiovascular drugs

Cardiovascular drugs such as angiotensin converting enzyme inhibitors (ACE-I, e.g. perindopril or quinapril and captopril), HMG-CoA reductase inhibitors (statins, e.g. atorvastatin or simvastatin, but not cerivastatin) or some beta- adrenoceptor blocking agents (beta-B, e.g. nebivolol or carvedilol, but not propranolol) apart from their basic mechanisms of action exert also pleiotropic effects. Here we assessed their in vivo pleiotropic endothelial properties measured as a thrombolytic response in arterial blood of anaesthetised Wistar rats, that was evoked by intravenous injections of a these drugs. Thrombolysis was associated with a rise in 6-keto-PGF(1alpha) levels in blood. ACE-I proved to be by two order of magnitude more potent thrombolytic agents and PGI(2) releasers than statins or beta-B. We hypothesize that in case of ACE-I [1, 2] it is the endocrine-like function of the pulmonary circulation [3, 4], which is responsible for bradykinintriggered, PGI(2)-mediated thrombolysis, whereas pleiotropic action of statins and of beta-B is due to their diffused stimulation of extrapulmonary vascular beds.