The effect of tunicamycin on prostacyclin (PGI(2)) receptors of neuronal hybrid cells.

The number of PG1(2) receptors in NCB-20 neuronal hybrid cells assayed by specific [(3)H]iloprost binding is substantially reduced when cells are cultured in the presence of tunicamycin, the specific inhibitor of protein N-glycosylation. The effect is reversible, dose and time dependent, and is on the number of receptors not their affinity. Tunicamycin was shown to have a selective effect on glycoprotein synthesis under these conditions with only slight effects on total protein synthesis.

Application of a frequency definition of ventricular proarrhythmia.

To differentiate spontaneous variability from proarrhythmia in patients with benign or potentially lethal ventricular arrhythmias, 495 patients with 2 or more Holter tracings during placebo therapy were evaluated. The Holter session with the highest frequency of ventricular premature complexes (VPCs) and ventricular tachycardia was compared with the first placebo recording. Patients were segregated by their baseline frequency of VPCs.

The role of calcium ion as a mediator of the effects of angiotensin II, catecholamines, and vasopressin on the phosphorylation and activity of enzymes in isolated hepatocytes.

Angiotensin II, catecholamines, and vasopressin are thought to stimulate hepatic glycogenolysis and gluconeogenesis via a cyclic AMP-independent mechanism that requires calcium ion. The present study explores the possibility that angiotensin II and vasopressin control the activity of regulatory enzymes in carbohydrate metabolism through Ca2+-dependent changes in their state of phosphorylation. Intact hepatocytes labeled with [32P]PO43- were stimulated with angiotensin II, glucagon, or vasopressin and 30 to 33 phosphorylated proteins resolved from the cytoplasmic fraction of the cell by electrophoresis in sodium dodecyl sulfate polyacrylamide slab gels.

Regulation of mitochondrial pyruvate carboxylation and gluconeogenesis in rat hepatocytes via an alpha-adrenergic, adenosine 3':5'-monophosphate-independent mechanism.

Experiments were performed to determine if catecholamines can regulate control points in the gluconeogenic pathway, such as mitochondrial pyruvate carboxylation and pyruvate kinase activity, via an alpha-adrenergic, adenosine 3':5'-monophosphate-independent mechanism. Of a number of alpha agonists tested, only norepinephrine, epinephrine, and phenylephrine caused an increase in mitochondrial pyruvate metabolism. The effects of catecholamines on pyruvate carboxylation were not attenuated by 1-propranolol which abolishes changes in cyclic nucleotide levels but were blocked by alpha antagonists such as ergotamine, phenoxybenzamine, and phentolamine.