Springer Online Journal Archives 1860-2000
Chemistry and Pharmacology
Summary The fasting level of plasma very low density lipoproteins (VLDL) was increased by 30 to 50% in 12 healthy male volunteers treated with daily oral doses of hydrochlorothiazide 100 mg, chlorthalidone 100 mg or furosemide 80 mg for 3 weeks in a cross-over trial. Hydrochlorothiazide and chlorthalidone, but not furosemide, caused a 10% increase in cholesterol in the low density lipoproteins (LDL), whereas triglycerides and phospholipids in this fraction remained unchanged. High density lipoproteins (HDL) were not affected by any of the diuretics. Free palmitic and oleic acid in plasma were also increased during the treatment, perhaps because of an accumulation of cyclic 3′5′-AMP due either to the inhibitory action of diuretics on phosphodiesterase, or to secondary activation of the sympathetic nervous systems. This would activate lipolysis in fat tissue, which in turn may induce VLDL synthesis in the liver. Each of the diuretics caused a similar rise of 20 to 30% in the mean plasma uric acid, the which could not be correlated with either triglycerides or cholesterol. Plasma sodium was increased by 2% only by furosemide, whereas potassium was decreased by 15 and 19% by hydrochlorothiazide and chlorthalidone, respectively, but not by furosemide. Mean plasma creatinine rose by 3.5% on treatment with furosemide, and by 6% with the other two diuretics. Mean body weight was reduced by 1,4 to 2,0% during treatment. No change in fasting blood sugar, plasma protein level or hematocrit was found.
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