الفهرس 
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Abstract
Lisinopril is an orally active angiotensin-converting enzyme (ACE) inhibitor which has been proven to be effective in blood pressure management in all grades of essential hypertension. The Food and Drug Administration (FDA) has approved lisinopril for the treatment of hypertension in adults and children aged six and up, as well as as an adjunctive therapy in the treatment of heart failure. It’s also approved by the FDA for treating ST-segment elevation myocardial infarction (STEMI) in hemodynamically stable patients within 24 hours to improve survival. Lisinopril also emerged as a well-tolerated active pharmaceutical ingredient (API) to improve cardiac function in patients with congestive heart failure (CHF) with crucial resistance to conventional therapy. Being a Biopharmaceutics classification system (BCS) class III drug, lisinopril is a hydrophilic drug showing poor membrane permeability and an estimated oral bioavailability of approximately 25%. It exerts its action via inhibition of angiotensin-converting enzyme preventing angiotensin I conversion to angiotensin II. Remarkably, lisinopril exhibits significant features making it different from the previously approved angiotensin converting enzyme inhibitors, captopril and enalapril. It has been issued to be safer and more effective in blood pressure lowering and CHF control than either captopril or enalapril. Unfortunately, the literature lacks information about the mechanism of intestinal membrane transport of lisinopril and how to tailor enhanced intestinal permeability according to its absorption pathway. The aim of this thesis is mainly to investigate the intestinal site dependent absorption of lisinopril employing in situ rabbit intestinal perfusion technique. Furthermore, involvement of carrier mediated transport of lisinopril may be assessed regarding its concentration dependent absorption profile. The study was extended to explore the effect of two selected permeability enhancers (piperine and zinc acetate di-hydrate) on lisinopril intestinal absorption. The tested enhancers were selected based on their different mechanisms of enhancing intestinal permeability providing an extra proof for the argued transport pathways of lisinopril. This may lay a cornerstone for subsequent elaboration of a suitable oral drug delivery systems of lisinopril. The proceeding sections summarize the studies performed to achieve this aim.