Metabolic effects of calcium antagonists in humans, with emphasis on carbohydrate, lipid, potassium, and uric acid homeostases.
Since metabolic side effects of conventional antihypertensive drugs could be one reason for the lack of improvement of cardiac morbidity and mortality, metabolic neutrality has become an important postulate of newer products such as the calcium antagonists (CA). Carbohydrate homeostasis--in spite of an anticipated deterioration derived from early in vitro experiments--has mostly been unaffected by CA therapy in humans, nondiabetic and diabetic. This was found in long-term studies in particular, whereas in acute or short-term trials with high dosages, minor alterations of insulin secretion and/or action were sometimes noted. These are negligible from a clinical point of view. Serum lipid profiles also were generally not disturbed by CA treatment, since most of the controlled long-term trials showed no change or even a potentially beneficial change. Minor lowering of plasma potassium levels during a CA regimen was exceptional and a rise of plasma uric acid values never reported; the latter may even decrease under certain circumstances. Thus, after reviewing more than 150 pertinent publications, we can state that the benefit of antihypertensive or antianginal treatment with a CA is in all likelihood not compromised by introducing known untoward metabolic cardiovascular risks.
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Medizinische Poliklinik, University of Berne, Switzerland.
Weidmann
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D002121:Calcium Channel Blockers / Q000009:adverse effects*; D050260:Carbohydrate Metabolism; D006706:Homeostasis / Q000187:drug effects*; D006801:Humans; D050356:Lipid Metabolism; D011188:Potassium / Q000378:metabolism*; D014527:Uric Acid / Q000378:metabolism*
D002121:Calcium Channel Blockers; D014527:Uric Acid; D011188:Potassium