Abstract

To the Editor: I enjoyed learning from the article by Lee et al1 about the possible relationship between ACE-inhibitor cough and the NO synthase (NOS) system. During the past decade, there has been some accumulation of data relating NOS to cardiovascular diseases and endocrinic effects. This enzyme, which is usually expressed in skeletal muscle and vascular endothelium, when knocked out in eNOS−/−mice has been shown to cause not only hypertension but also insulin resistance and hyperlipidemia, metabolic derangements not found in other hypertension model mice and rats.2 Sustained hyperinsulinemia in rats was shown to cause insulin resistance, hypertension, and impairment of eNOS activity. Further inhibition of eNOS by a specific inhibitor in these rats increased the severity of their systolic blood pressure (from 134 to 158 mm Hg with insulin alone and to …

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