Angiotensin-converting enzyme diuretics

Thiazide diuretics have a venerable history as antihypertensive agents until the advent of the angiotensin-converting enzyme (ACE) inhibitors this class of drugs completely dominated first line therapy for hypertension. The size of thi.s market led until surprisingly recently to the syntheses of new sulfonamides related to the thiazides. Preparation of one of the last of these compounds starts by exhaustive reduction of the Diels-Alder adduct from cyclopentadiene and malei-mide (207). Nitrosation of the product (208), followed by reduction of the nitroso group of 209,... 

Until recently, the cardiotonics and a diuretic were the treatment of choice for HE However, other dragp such as the angiotensin-converting enzyme (ACE) inhibitors, and beta blockers have become the treatment of choice during the last several years. See Figure 39-1 for an example of a method of determining treatment for left ventricular systolic dysfunction. See Chapters 23, 42, and 46 for more information on the beta blockers, ACE inhibitors, and diuretics, respectively. 

Other medications (e.g., angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and diuretics)... 

Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs. diuretic The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2002 288(23) =2981-2997. 

Medications can increase the risk of hyperkalemia in patients with CKD, including angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, used for the treatment of proteinuria and hypertension. Potassium-sparing diuretics, used for the treatment of edema and chronic heart failure, can also exacerbate the development of hyperkalemia, and should be used with caution in patients with stage 3 CKD or higher. 

Hypotonic hyponatremia with an increase in ECF is also known as dilutional hyponatremia. In this scenario, patients have an excess of total body sodium and TBW however, the excess in TBW is greater than the excess in total body sodium. Common causes include CHF, hepatic cirrhosis, and nephrotic syndrome. Treatment includes sodium and fluid restriction in conjunction with treatment of the underlying disorder—for example, salt and water restrictions are used in the setting of CHF along with loop diuretics, angiotensin-converting enzyme inhibitors, and spironolactone.15... 

Angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors not only cause vasodilation (1 TPR), but also inhibit the aldosterone response to net sodium loss. Normally, aldosterone, which enhances reabsorption of sodium in the kidney, would oppose diuretic-induced sodium loss. Therefore, coadministration of ACE inhibitors would enhance the efficacy of diuretic drugs. 

Most patients with stage 1 hypertension should be treated initially with a thiazide diuretic, angiotensin-converting enzyme (ACE) inhibitor, angio-... 

Elevated blood pressure is common after ischemic stroke, and its treatment is associated with a decreased risk of stroke recurrence. The Joint National Committee and AHA/ASA guidelines recommend an angiotensin-converting enzyme inhibitor and a diuretic for reduction of blood pressure in patients with stroke or TIA after the acute period (first 7 days). Angiotensin II receptor blockers have also been shown to reduce the risk of stroke and should be considered in patients unable to tolerate angiotensinconverting enzyme inhibitors after acute ischemic stroke. 

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have shown efficacy in preventing the clinical progression of renal disease in patients with type 2 DM. Diuretics are frequently necessary due to volume-expanded states and are recommended second-line therapy. 

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are generally recommended for initial therapy. Many patients require multiple agents, so diuretics, calcium channel blockers, and /)-blockers are useful as second and third agents. 

Zestril contains lisinopril, an angiotensin-converting enzyme inhibitor. Angiotensin-converting enzyme inhibitors tend to retain potassium, thereby counteracting the potassium loss caused by the thiazide diuretic bendroflumethiazide. 

Concomitant administration of methotrexate and Voltarol, a proprietary preparation of diclofenac, a non-steroidal anti-inflammatory drug, may result in accumulation of methotrexate as its excretion is reduced. The use of diclofenac and diuretics such as bendroflumethiazide may increase the risk of nephrotoxicity. Concomitant use of alcohol and an angiotensin-converting enzyme inhibitor such as lisinopril (Zestril) may result in an enhanced hypotensive effect. Alcohol and the benzodiazepine diazepam (Valium) may result in enhanced sedation. 

Angiotensin-converting enzyme inhibitors should be used with caution in patients taking diuretics because of an enhanced hypotensive effect. Angiotensin-converting enzyme inhibitors should also be used with caution in patients with renal impairment. Renal function needs to be monitored in patients with renovascular disease. 

Concomitant administration of diuretics and angiotensin-converting enzyme (ACE) inhibitors results in enhanced hypotensive effect. Blood pressure monitoring is required, therefore, if patients who are on diuretics are started on ACE inhibitors. The ACE inhibitor should be initiated in the evening to avoid falls d ue to hypotension. 

Moreover, whether or not hypertension is caused by an elevated level of renin or other reasons, angiotensin-converting enzyme inhibitors lower both systolic and diastolic arterial pressure in hypertensive patients, and their effects are enhanced by diuretics. Angiotensin-converting drugs of this series (captopril, enalapril) are effective antihypertensive drugs used both independently and in combination with other drugs to treat all types of hypertension as well as to treat cardiac insufficiency. 

Ketanserin should not be combined with drugs that prolong the QT interval, e.g. class la anti-arrhythmics, amiodarone, sotalol, erythromycin. The risk of torsade de pointes secondary to hypokalaemia is increased when ketanserin is combined with thiazides or loop diuretics without concomitant use of a potassium-sparing diuretic or an angiotensin-converting enzyme (ACE) inhibitor, a 1 Antagonists... 

Hyperkalaemia, not surprisingly, is the most important side effect of these drugs and can be dangerous in patients who are taking K-i- supplements or other K-i--sparing diuretics. Concomitant use of angiotensin-converting enzyme (ACE) inhibitors and NSAIDs can also exacerbate hyperkalaemia. 

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