Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha-Adrenergic blockade with phentolamine or prazosin but not beta-adrenergic blockade reduces premature ventricular complexes and abolished ventricular fibrillation induced by coronary artery ligation or reperfusion in cats. The protective influences were independent of regional coronary flow or systemic hemodynamics. Efferent sympathetic nerve stimulation increased the idioventricular rate (IVR) prior to myocardial ischemia, a response blocked by propranolol, whereas during reperfusion the increased IVR was abolished only by alpha-blockade. Enhanced alpha-adrenergic responsiveness during reperfusion was also apparent with the alpha-agonist methoxamine. More recently we have demonstrated that alpha-adrenergic receptors, assessed by ligand binding with 3H-prazosin, increased nearly twofold in ischemic myocardium by 30 minutes (Bmax = 14 + 2 to 27 + 3 fmol/mg prot) and remain elevated during early reperfusion (12 + 1 to 18 + 1) before returning to control values by 15 minutes after reperfusion. 3H-DHA binding or Na+- -K+ adenosine triphosphatase activity was not altered at any time, indicating the specificity of the alteration. Thus enhanced alpha-adrenergic receptors and suggests the potential use of alpha-adrenergic blockade as one intervention to alleviate these malignant dysrhythmias.
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PMID:Enhanced alpha-adrenergic responsiveness in ischemic myocardium: role of alpha-adrenergic blockade. 611 77

The structure-toxicity relationship of monoketones, a class of organic solvents widely used in industry, was investigated with respect to their in vitro effects on synaptosomal membrane proteins. The toxic parameters used were Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase), a well-known marker enzyme often used as a membrane toxicity model, and 3H-dihydroalprenolol (3H-DHA)-labeled beta-adrenergic receptor binding that has been shown to be vulnerable to solvent-induced changes in membrane fluidity. In vitro treatments with 12 kinds of monoketones (carbon chain length from 3-10) dose-dependently inhibited both 3H-DHA binding to mouse synaptosomes and Na(+)-K(+)-ATPase activity. The potency of inhibition (IC50) for both the two parameters was linearly related to n-octanol/water partition coefficient and synaptosome/buffer partition coefficient of the test compounds. Additions of monoketones did not significantly alter the number of 3H-DHA binding sites but markedly decreased their affinity. In each monoketone, the IC50 values for 3H-DHA binding and Na(+)-K(+)-ATPase activity were generally within the same range. The anisotropy of fluorescence probe 1,6-diphenyl-1,3,5-hexatriene-labeled synaptosomal membranes was dose-dependently decreased by the monoketones, implying increased membrane fluidity. These results indicate that increasing lipophilicity of monoketones results in increased solvent penetration of synaptic membrane preparations, leading to conformational changes in membrane structure and increased ability to inhibit both neuroreceptor binding and enzyme activity. The present data confirm the importance of the lipid micro-environment of membranes in maintaining the normal functions of membrane-bound proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Structure-toxicity relationship of monoketones: in vitro effects on beta-adrenergic receptor binding and Na(+)-K(+)-ATPase activity in mouse synaptosomes. 827 28