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Skeletal muscle depressed calcium and phosphofructokinase in chronic heart failure are upregulated by captopril ‐ a double‐blind, placebo‐controlled study
Author(s) -
SYLVÉN C.,
JANSSON E.,
CEDERHOLM T.,
HILDEBRAND I. L.,
BEERMANN B.
Publication year - 1991
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1991.tb00326.x
Subject(s) - captopril , medicine , endocrinology , phosphofructokinase , skeletal muscle , placebo , angiotensin converting enzyme , calcium , glycolysis , blood pressure , metabolism , alternative medicine , pathology
. The effects of the angiotensin converting enzyme inhibitor captopril, after treatment for 5‐6 weeks with 25 mg t.i.d., were studied in 12 patients with stable moderate heart failure. Five patients received placebo treatment, and the two groups were comparable at baseline. Angiotensin II levels decreased in response to captopril therapy. Skeletal muscle potassium, magnesium and chloride levels did not differ from reference values. Calcium was subnormal ( P < 0.0001), but increased to the reference range during captopril treatment. Phosphofructokinase, a rate‐limiting glycolytic enzyme, was in the lower reference range and increased ( P < 0.04) in response to captopril therapy. In conclusion, stable moderate heart failure is associated with low levels of skeletal muscle calcium and phosphofructokinase activity, these metabolic changes tending to return to normal levels with captopril treatment.