PubMed · 143148
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A A Boldyrev, O D Lopina. [Sarcoplasmic reticulum].. https://pubmed.ncbi.nlm.nih.gov/143148/
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Patients with hypercholesterolemia have impaired endothelium-dependent vasodilation due to decreased nitric oxide activity. The present study aimed to determine whether this form of endothelial dysfunction is related to enhanced extracellular breakdown of nitric oxide by superoxide anions. To this end, the vascular responses to acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct smooth muscle dilator) were studied before and after combined administration of copper-zinc superoxide dismutase (a scavenger of superoxide anions with poor intracellular penetrance; 6,000 U/min) in 20 normal controls (11 men and 9 women, age 50 +/- 6 years) and in 20 hypercholesterolemic patients (10 men and 10 women, age 49 +/- 9 years). Drugs were infused into the brachial artery and the response of the forearm vasculature was measured by plethysmography. The vasodilator response to acetylcholine was significantly blunted in hypercholesterolemic patients compared with normal controls (maximal flow 8.8 +/- 2 vs 12.7 +/- 3 ml/min/100 ml, respectively; p < 0.03); however, no difference was observed in the response to sodium nitroprusside (9.7 +/- 2 and 9.5 +/- 3 ml/min/100 ml). In normal controls, the infusion of superoxide dismutase did not significantly modify the response to acetylcholine (maximal flow 12.7 +/- 3 vs 12.1 +/- 3 ml/min/100 ml before and after superoxide dismutase, respectively). Similarly, in hypercholesterolemic patients, the infusion of superoxide dismutase did not alter the response to acetylcholine (maximal flow 8.8 +/- 2 and 8.9 +/- 2 ml/min/100 ml). A subset of 19 subjects (8 normal and 11 patients) received a 60-minute infusion of superoxide dismutase at 24,000 U/min without alteration in their response to acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)
This study showed that endothelial dysfunction is present in men 3 to 6 months after myocardial infarction, but was unable to show any improvement in endothelial function after 3 months of therapy with vitamin E 800 IU/day. Further studies are necessary to determine whether higher doses or a longer course of vitamin E, or whether other antioxidant agents with or without lipid-modifying activity, would improve endothelial function.
The regulation of the synthesis of acetylcholine and phosphatidylcholine in rat sympathetic neurons was examined in the context of cholinergic differentiation. We demonstrate that the activities of choline acetyltransferase (ChAT) and choline kinase (CK) are inversely affected by treatment of sympathetic neurons with retinoic acid, utilized as an agent that induces cholinergic differentiation. Whereas ChAT specific activity increased 2- to 4-fold after 12 days of treatment with 5 microM retinoic acid, CK specific activity decreased by 25-30%. These changes in enzyme activities were essentially reflected in the incorporation of [methyl-3H]choline into ACh and the metabolites of the CDP-choline pathway for phosphatidylcholine synthesis. When sympathetic neurons were treated under high potassium conditions (50 mM) for 12 days, the specific activity of CK increased 1.3-fold whereas the activity of ChAT decreased by up to 90%. Furthermore, experiments in which the incorporation of [methyl-3H]choline into ACh and the metabolites of the CDP-choline pathway was measured in the absence of Na+ or in the presence of hemicholinium-3 (HC-3), demonstrate that CK has access to the same pool of choline utilized by ChAT. These results provide evidence that the activities of ChAT and CK may be inversely regulated during the process of cholinergic differentiation.