Clinical Pharmacology of ACE Inhibition

Nussberger, Jürg; Waeber, Bernard; Brunner, Hans R.

doi:10.1159/000174555

Cited by 13 publications

(8 citation statements)

References 10 publications

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“…As seen in previous studies [13,15,23], resting and exercising plasma renin activity were markedly increased by ACE-inhibitor treatment. The addition of nadolol suppressed the enalapril-induced increase in plasma renin activity at rest and during exercise, and reduced plasma aldosterone levels.…”

Section: Discussionsupporting

confidence: 82%

Enalapril versus combined enalapril and nadolol treatment: Effects on blood pressure, heart rate, humoral variables, and plasma potassium at rest and during exercise in hypertensive patients

Sullivan

Daly

O’Connor

1992

Cardiovasc Drug Ther

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The effect of enalapril alone and in combination with nadolol on resting and exercising blood pressure, heart rate, plasma renin activity, aldosterone, noradrenaline, and potassium levels was studied in 10 hypertensive patients (diastolic blood pressure between 95 and 114 mmHg). Patients received placebo for 4 weeks, enalapril (mean daily dose 24.5 mg) for 8 weeks, and nadolol, 40 mg once daily, was added for the remaining 8 weeks of the study. Exercise testing (modified Bruce, treadmill) was conducted at the end of the placebo run-in phase and at the end of each treatment period. Enalapril reduced resting and exercising blood pressure independent of any change in heart rate: This effect was increased with combination treatment. Plasma renin activity at rest and during exercise was increased by enalapril. Combination treatment attenuated this response and significantly reduced plasma aldosterone. Neither treatment had any effect on plasma noradrenaline levels. Resting plasma potassium levels were increased with combination treatment, whereas both treatment regimens increased plasma potassium levels during exercise. There were no clinically relevant episodes of hyperkalemia. Further investigation is required to qualify the nature of the blood pressure and plasma potassium response with combination treatment.Cardiovasc Drugs Ther 1992;6:261-265

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Section: Discussionsupporting

confidence: 82%

Enalapril versus combined enalapril and nadolol treatment: Effects on blood pressure, heart rate, humoral variables, and plasma potassium at rest and during exercise in hypertensive patients

Sullivan

Daly

O’Connor

1992

Cardiovasc Drug Ther

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“…ACE inhibitors block angiotensin II production via blockade of the converting enzyme. 27 The converting enzyme is also responsible for the catabolism of other peptides, such as bradykinin. 27 Furthermore, alternative pathways exist for the production of angiotensin II (trypsin, cathepsin, and chymase).…”

Section: Is It Time For Combination Therapy?mentioning

confidence: 99%

“…27 The converting enzyme is also responsible for the catabolism of other peptides, such as bradykinin. 27 Furthermore, alternative pathways exist for the production of angiotensin II (trypsin, cathepsin, and chymase). 28 ARBs, acting through blockade of the angiotensin type 1 receptor, work downstream from angiotensin II production to block its effects.…”

Section: Is It Time For Combination Therapy?mentioning

confidence: 99%

Combination Therapy With Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Antagonists in the Treatment of Patients With Type 2 Diabetes Mellitus

Rosner

Okusa²

2003

Arch Intern Med

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Aggressive therapy for patients with type 2 diabetes mellitus and renal disease is warranted given the natural history of this disease. Although antagonizing the renin-angiotensin system is clearly important, how this is accomplished is of considerable controversy. On the one hand, recent clinical trials of patients with type 2 diabetes mellitus with renal disease demonstrate unequivocally the renal protective effect of angiotensin receptor blockers (ARBs). Although the results of the recently published LIFE trial are encouraging, inconsistencies have been observed with ARBs in reducing cardiovascular end points. On the other hand, angiotensin-converting enzyme inhibitors have a dramatic effect in reducing cardiovascular events but have not been shown convincingly to reduce progression of renal disease in patients with type 2 diabetes mellitus. These studies leave us in a quandary as to the optimal initial treatment regimen for patients with type 2 diabetes mellitus and renal disease despite the recent recommendations from the American Diabetes Association (Alexandria, Va). Given the fact that many of these individuals will require administration of multiple antihypertensive agents, perhaps the initial treatment with a combination of an ARB and angiotensin-converting enzyme inhibitor affords optimal cardiovascular and renal protection for patients with type 2 diabetes mellitus and renal disease. Future clinical trials should be designed to address this issue.

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“…ACE inhibitors block the RAAS preventing the conversion of inactive angiotensin I to active ANG-II,18and may improve portal hypertension. However, concerns have been raised about their safety because of arterial hypotension and deterioration of renal function.…”

mentioning

confidence: 99%

Angiotensin converting enzyme inhibitors and angiotensin II antagonists as therapy in chronic liver disease

Vlachogiannakos

An-li

Patch

et al. 2001

Gut

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Clinical Pharmacology of ACE Inhibition

Cited by 13 publications

References 10 publications

Enalapril versus combined enalapril and nadolol treatment: Effects on blood pressure, heart rate, humoral variables, and plasma potassium at rest and during exercise in hypertensive patients

Enalapril versus combined enalapril and nadolol treatment: Effects on blood pressure, heart rate, humoral variables, and plasma potassium at rest and during exercise in hypertensive patients

Combination Therapy With Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Antagonists in the Treatment of Patients With Type 2 Diabetes Mellitus

Angiotensin converting enzyme inhibitors and angiotensin II antagonists as therapy in chronic liver disease

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