ABSTRACT
This chapter discusses the drugs which have been employed in cirrhosis to specifically counteract the activated renin-aldosterone axis. The pharmacological inhibition of the renin-angiotensin system can occur at different sites: release of renin from the juxtaglomerular apparatus; inhibition of angiotensin-converting enzyme activity; blockade of receptors for angiotensin II. Most of the available information on the effect of P-adrenergic receptor blockade in patients with cirrhosis is based on the results obtained by propranolol administration. Therefore, the present discussion will focus on this drug, recalling variant effects by other ß-adrenergic antagonists when relevant. The mechanisms underlying propranolol influence on renal function of cirrhotic patients are not completely understood. The maintenance of renal perfusion has been attributed to the suppression of the renin-angiotensin system and/or activation of vasodilating substances, such as prostaglandins or bradykinin. Captopril was the first available orally effective inhibitor of the angiotensin -converting enzyme.
