Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.1 (Mg2+-ATPase)
 1,484 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prazosin has been used in the treatment of congestive heart failure. It is, however, not known whether prazosin gives only haemodynamic benefit or if it also produces a decrease in the cardiac sarcolemmal Na+-K+-ATPase which has been reported to be increased in the failing heart. The present investigation deals with the effect of 3 months of prazosin treatment in dogs with 3 months of induced mitral insufficiency (MI) on the sarcolemmal Na+-K+-ATPase activity. The dogs were divided into four groups each comprising of five dogs. A--normal; B--3 months of MI; C--6 months of MI; D--3 months of prazosin treatment after 3 months of MI. Three months of MI produced a decrease in the dp/dt and an increase in the end-diastolic pressure of left ventricle but no change in the index of left ventricular contractility and cardiac index. Also there was no change in the sarcolemmal Na+-K+-ATPase. There was a significant decrease in the index of left ventricular contractility and cardiac index and an increase in the LVEDP associated with a significant increase in the left ventricular sarcolemmal Na+-K+-ATPase at 6 months of MI. Sarcolemmal Mg2+-ATPase of both ventricles increased after 6 months of MI the significance of which is not known as yet. There was no change in the sarcolemmal Na+-K+-ATPase of the nonfailing right ventricle. Prazosin treatment prevented the deterioration of the left ventricular contractility and function and also prevented the increase in the sarcolemmal Na+-K+-ATPase observed in failing heart.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovasc Res 1985 Jul
PMID:Effect of prazosin treatment on the cardiac sarcolemmal ATPase in failing heart due to mitral insufficiency in dogs. 299 Jul 14

Vanadate is a potent inhibitor of Na+,K+-ATPase derived from bovine aorta. The Ca2+, Mg2+-ATPase of the same preparation was inhibited at 10 times higher concentrations. Compared with [3H]ouabain, 48V bound quickly to bovine aortic microsomes. Equilibrium binding experiments revealed one high-affinity, low-capacity and one low-affinity binding site for 48V, whereas [3H]ouabain possessed only one binding site of high affinity. A high NADH-vanadate reductase activity was measured in the same preparation, suggesting that, in this tissue, vanadate may be converted to vanadyl, a form to which the Na+,K+-ATPase is relatively insensitive. An increase in the contractile force of isolated rabbit aorta was measured with the following potency: phenylephrine greater than ouabain greater than vanadate. The order in intrinsic activity was as follows: phenylephrine congruent to ouabain greater than vanadate. The action of vanadate was rapid in onset and stable over several hours, while that of ouabain was slow and transitory. Vanadate increased tension in isolated rabbit veins to an extent similar to phenylephrine, but at concentrations two orders of magnitude higher. Vanadate action decreased with decreasing (Ca2+)0, but remained constant at a constant ratio of (Ca2+)0/(Na+)2(0). Vanadate-induced increases in tension were decreased by verapamil by about 43% and persisted in a solution in which Na+ was replaced by Li+. Vanadate increased electrically stimulated contractions. It is concluded that most of the effect of vanadate is due to an increase in calcium influx into the smooth muscle cell and that the effect of vanadate on Na+,Ca2+ exchange is of minor importance.
J Cardiovasc Pharmacol
PMID:Effects of vanadate on isolated vascular tissue: biochemical and functional investigations. 618 8

In vitro and ex vivo interactions of betaadrenoceptor blocking drugs, antihistamines and chloroquine with blood platelets and polymorphonuclear leukocytes resulted in different alterations of regulatory functions of these blood cells. Inhibition of platelet aggregation, arachidonate regulatory pathway, 5-hydroxytryptamine transportation, removal of platelet membrane receptors, inhibition of second messenger pathways at subcellular level and suppression of phagocytosis are indicative of nonreceptor rather than specific receptor interactions. Binding of drugs with biomembranes is reversible depending on the ionic charge of the molecule and hydrophobicity of the bilayer, partition coefficient, pH and pKa of the amphiphilic molecules and other physico-chemical properties of amphiphilic drugs. Alterations in the drug molecule structure alters the drug-phospholipid binding profile. Any change in the metabolism of membrane phospholipids directly or indirectly influences one or more of the important components of the phospholipid-signalling pathway. In addition to changes in phospholipase A, C and D activities, protein kinase C, calmodulin-phosphodiesterase, Ca2+,Mg2+-ATPase, Na+,K+-ATPase and other messengers were found to be changed in cells and tissue after cationic amphiphilic drug (CAD) administration. Although not much has been understood of the mechanism by which some CAD affect immune functions, there are good reasons to suggest that these effects might occur. CADs share sufficient similarities in their structure even though they come from diverse pharmacological classes. CADs affect ion transport, immune functions, tumour growth, serotonin metabolism and several other functions in the body. Extensive therapeutic use and associated side effects have generated a great deal of interest in understanding the nonreceptor interactions with CADs.
Cardiovasc Hematol Agents Med Chem 2006 Jul
PMID:Antiplatelet and antileukocyte effects of cardiovascular, immunomodulatory and chemotherapeutic drugs. 1684 9