Summary The advent of the increasing use of different angiotensin-converting enzyme (ACE) inhibitors for the treatment of hypertension and cardiac failure has resulted in intense interest in the renin-angiotensin system (RAS) and its manipulation for therapeutic gain, and thus more patients will present for surgical anaesthesia while on maintenance therapy with these agents. The RAS is increasingly described in terms of systemic and tissue components. The systemic component is important in maintaining cardiovascular and body fluid homoeostasis, and is activated through renin release by the juxtaglomerular cells of the kidney in response to signs of disequilibrium. Angiotensin I is formed from renin substrate and is converted by ACE to angiotensin II, the major mediator of this system, which in turn stimulates aldosterone release from the adrenal cortex. In addition, aldosterone can be released independently in response to changes in plasma potassium concentration. The release of these hormones is regulated through various feedback mechanisms. The role of the tissue RAS is not clear but has been found to be present in many organ systems and is increasingly seen as the major site of action of ACE inhibitor drugs. The first oral ACE inhibitor, captopril, introduced in 1977, was followed by enalapril (which can also be administered intravenously) and lisinopril. These agents inhibit the conversion of angiotensin I to angiotensin II. ACE inhibitors also inhibit the inactivation of bradykinin, a vasodilator, which in turn enhances vasodilatory prostaglandin formation. ACE inhibitors have been found increasingly useful in the therapy of hypertension and cardiac failure, and new indications for their use are under investigation. The effect of anaesthesia on the RAS has undergone limited study. Indications are that neither the RAS nor ACE are directly affected by anaesthetics. Preoperative therapy with ACE inhibitors has been associated with severe hypotension after induction of and during anaesthesia. In addition, the critical role of the RAS in the defence of blood loss is becoming apparent in patients receiving ACE inhibitors. In aortic surgery, however, ACE inhibition may be renoprotective, and experimentally these drugs have been shown to reduce myocardial infarct size after coronary occlusion in dogs. Thus, further studies are required to determine the exact role of ACE inhibitors in the perioperative period.