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   <subfield code="a">Effects of beta-blockers on HMG CoA reductase and LDL receptor activity in cultured human skin fibroblasts</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Hiroshi Yoshida, Michio Suzukawa, Toshitsugu Ishikawa, Hideki Shige, Eisuke Nishio, Hiroshi Hosoai, Makoto Ayaori, Haruo Nakamura]</subfield>
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   <subfield code="a">Summary: Previous reports, based on clinical trials and animal experiments, suggest that beta-blockers may be useful in the prevention of atherosclerosis. Betaxolol, a new beta1-selective blocker, was shown to decrease plasma total and LDL cholesterol levels or to have no adverse effect on those [1-4]. While many reports deal with the metabolism of triglyceride and high density lipoprotein, fewer publications about cholesterol metabolism are currently available. To clarify the mechanism by which beta-blockers affect lipid metabolism, we examined the effects of beta-blockers on HMG CoA reductase and LDL receptor activity in cultured human skin fibroblasts. L-propranolol, a nonselective betablocker, increased HMG CoA reductase activity and decreased LDL receptor activity. However, d-propranolol had no major effects on HMG CoA reductase activity. These results suggest that beta-blockers act on HMG CoA reductase through the beta receptors. Beta1-blocking action should decrease HMG CoA reductase activity and increase LDL receptor activity. In fact, betaxolol, a beta1-selective blocker, decreased HMG CoA reductase activity and increased LDL receptor activity, but metoprolol had no major effect. We speculate that the discrepancy between betaxolol and metoprolol in the effect on HMG CoA reductase and the LDL receptor might be due to the difference of the extent of beta1-selectivity. We conclude that beta1-selective blockers are antihypertensive agents potentially valuable in the prevention of atherosclerosis.</subfield>
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   <subfield code="a">Yoshida</subfield>
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   <subfield code="u">lst Department of Internal Medicine, National Defense Medical College, Saitma, Japan</subfield>
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