Lisinopril significantly reduces left ventricular (LV) end-diastolic pressure (EDP), pulmonary capillary wedge pressure (PCWP) and end-diastolic stress, addition of atenolol to Lisinopril further reduces EDP and PCWP. [1] Lisinopril is a structural homologue of enalaprilat, differing only in the second amino acid side chain. Lisinopril inhibits Angiotensin-converting enzyme (ACE) in vitro, as well as after parenteral and oral administration to humans; its oral bioavailability is only 25-29%, but it has a longer duration of action than enalapril. [2]

Lisinopril treated SHR rats has significantly raised total cholesterol levels compared to untreated spontaneously hypertensive rats (SHR) rats (+27%), but not compared to lisinopril treated Wistar Kyoto rats (WKY) rats. [3] Lisinopril is a long-acting angiotensin-converting enzyme inhibitor which blocks the renin-angiotensin system (RAS) and reduces systemic blood pressure in rats. Lisinopril reduces the hydroxyproline level and inhibits accumulation of collagens in the pulmonary tissue of the treatment group (paraquat + lisinopril) and per-treatment group (lisinopril + paraquat) in rats. [4] Lisinopril results in preserved ultrafiltration volume (UF), glucose reabsorption (D 1 /D 0 glucose) and peritoneal thickness in rats. [5] Lisinopril (0.2 mg/kg twice a day for 10 days) protects the cell membrane integrity and lessens free radical-induced oxidant stress in guinea pig hearts. [6]