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W Krone

Publications and source records attributed to W Krone.

202 records · Page 12Linked to original sources
PubMedDate not supplied

Compactin inhibits cholesterol synthesis in lymphocytes and intestinal mucosa from patients with familial hypercholesterolaemia.

Compactin (2000 nmol/l), a potent competitive inhibitor of the rate-determinign enzyme for cholesterol synthesis (3-hydroxy-3-methyl-glutaryl coenzyme-A reductase), inhibited by about 90% cholesterol synthesis from 14C-acetate in isolated lymphocytes from healthy control and from patients heterozygous for familial hypercholesterolaemia (F.H.). In isolated intestinal mucosa, a physiologically important tissue for cholesterol synthesis, compactin (2000 nmol/l) suppressed cholesterol synthesis by approximately 50% in controls and F.H. patients. Compactin or its derivatives may prove to be useful in the treatment of hypercholesterolaemia.

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PubMedDate not supplied

Effects of adrenergic antihypertensive drugs on sterol synthesis in freshly isolated human mononuclear leukocytes.

The effects of the adrenergic antihypertensive drugs propranolol, clonidine, alpha-methyldopa, urapidil, indoramin, and prazosin on the relative rate of sterol synthesis were studied in freshly isolated human mononuclear leukocytes. Incubation of cells for 6 h in a medium containing lipid-depleted serum led to a threefold increase in the incorporation of [14C]acetate or tritiated water into sterols. (-)-Epinephrine added at zero time to the incubation medium inhibited the relative rate of sterol synthesis by 32% at a concentration of 1 mumol/L. The non-specific beta-blocker propranolol, added at equimolar concentrations, almost abolished the epinephrine-induced suppression. The beta-blocker per se had no effect on the incorporation of [14C]acetate into sterols up to a concentration of 1 mumol/l. The alpha 2-agonist clonidine and alpha-methyldopa, added in increasing concentrations at zero time, inhibited the relative rate of sterol synthesis, yielding a sigmoidal log dose-effect curve. The suppression was 43 and 24%, respectively, at a concentration of 0.1 mmol/L. The alpha 1-antagonists indoramin, prazosin, and urapidil, up to a concentration of 10 mumol/L, had no effect per se, or on the epinephrine-induced suppression of the relative synthesis rate of sterols. The results give evidence that various antihypertensive adrenergic drugs, depending on their action on beta- or alpha-adrenergic receptors, have different effects on cholesterol biosynthesis and therefore may affect cellular cholesterol homeostasis.

Adrenergic alpha-Agonists↗