Benazepril is a prodrug which is metabolized by the liver into its active form benazeprilat via cleavage of the drug's ester group. Benazepril and Benazeprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and animals. Benazeprilat has much greater ACE inhibitory activity than does Benazepril. It is indicated for the treatment of hypertension. It may be used alone or in combination with thiazide diuretics. Adverse reactions reported in controlled clinical trials and rarer events seen in post-marketing experience, include the following: Stevens-Johnson syndrome, pemphigus, apparent hypersensitivity reactions (manifested by dermatitis, pruritus, or rash), photosensitivity, and flushing, nausea, pancreatitis, constipation, gastritis, vomiting, and melena, thrombocytopenia and hemolytic anemia, anxiety, decreased libido, hypertonia, insomnia, nervousness, and paresthesia. Patients on diuretics, especially those in whom diuretic therapy was recently instituted, may occasionally experience an excessive reduction of blood pressure after initiation of therapy with Benazepril. Increased serum lithium levels and symptoms of lithium toxicity have been reported in patients receiving ACE inhibitors (including benazepril) during therapy with lithium.

Nisoldipine is a 1,4-dihydropyridine derivative with an outstanding vascular selectivity. As a specific calcium antagonist, it shortens the action potential and causes electromechanical uncoupling in ventricular myocardium. However, this effect, resulting in a negative inotropic action, appears at 100–1000 times higher concentrations of nisoldipine in comparison with its inhibition of calcium-dependent vascular contractions. Detailed analyses of pharmacological effects revealed additional properties such as enhancement of sodium excretion, an interaction with the reninangiotensin-aldosterone system and a protective effect against acute renal ischaemia, that may contribute to its therapeutic efficacy. Nisoldipine was developed at Bayer then licensed to Zeneca and marketed in the United States as SULAR. SULAR is indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive agents. The mechanism of the therapeutic effect of nisoldipine is complex. It involves a decrease of the total peripheral vascular resistance (reduction of afterload) and an increase in coronary blood flow. Moreover, nisoldipine obviously normalises the impaired volume homoeostasis by improving renal function and thus reduces the need for activation of the ANP system. In the advanced stages of hypertension, nisoldipine prevents deleterious calcium overload and the resulting tissue damage.

Benazepril is a prodrug which is metabolized by the liver into its active form benazeprilat via cleavage of the drug's ester group. Benazepril and Benazeprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and animals. Benazeprilat has much greater ACE inhibitory activity than does Benazepril. It is indicated for the treatment of hypertension. It may be used alone or in combination with thiazide diuretics. Adverse reactions reported in controlled clinical trials and rarer events seen in post-marketing experience, include the following: Stevens-Johnson syndrome, pemphigus, apparent hypersensitivity reactions (manifested by dermatitis, pruritus, or rash), photosensitivity, and flushing, nausea, pancreatitis, constipation, gastritis, vomiting, and melena, thrombocytopenia and hemolytic anemia, anxiety, decreased libido, hypertonia, insomnia, nervousness, and paresthesia. Patients on diuretics, especially those in whom diuretic therapy was recently instituted, may occasionally experience an excessive reduction of blood pressure after initiation of therapy with Benazepril. Increased serum lithium levels and symptoms of lithium toxicity have been reported in patients receiving ACE inhibitors (including benazepril) during therapy with lithium.

Benazepril is a prodrug which is metabolized by the liver into its active form benazeprilat via cleavage of the drug's ester group. Benazepril and Benazeprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and animals. Benazeprilat has much greater ACE inhibitory activity than does Benazepril. It is indicated for the treatment of hypertension. It may be used alone or in combination with thiazide diuretics. Adverse reactions reported in controlled clinical trials and rarer events seen in post-marketing experience, include the following: Stevens-Johnson syndrome, pemphigus, apparent hypersensitivity reactions (manifested by dermatitis, pruritus, or rash), photosensitivity, and flushing, nausea, pancreatitis, constipation, gastritis, vomiting, and melena, thrombocytopenia and hemolytic anemia, anxiety, decreased libido, hypertonia, insomnia, nervousness, and paresthesia. Patients on diuretics, especially those in whom diuretic therapy was recently instituted, may occasionally experience an excessive reduction of blood pressure after initiation of therapy with Benazepril. Increased serum lithium levels and symptoms of lithium toxicity have been reported in patients receiving ACE inhibitors (including benazepril) during therapy with lithium.