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

Cardiomyopathic hamsters (UM-X7.1) show clinical signs of congestive heart failure and an abnormal EKG pattern. The sarcolemmal fraction obtained from the failing hearts at advanced stages of myopathy exhibited no change in the basal adenylate cyclase activity; however, the activity of this enzyme in the presence of catecholamines or NaF was lower in the failing heart sarcolemma than that in the control. The activities of Ca2+-ATPase, Mg2+-ATPase, and Na+-K+-ATPase in the failing heart sarcolemma were also less than the control values. These results suggest an association of membrane defect with heart failure.
 ...
PMID:Membrane alteration in failing hearts of cardiomyopathic hamsters. 12 77

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)
 ...
PMID:Effect of prazosin treatment on the cardiac sarcolemmal ATPase in failing heart due to mitral insufficiency in dogs. 299 Jul 14

An X-linked recessive disease is reported in a large pedigree. The disease is characterised by a triad of dilated cardiomyopathy, neutropenia and skeletal myopathy. The untreated patients, all boys, died in infancy or early childhood from septicemia or cardiac decompensation. Ultrastructural abnormalities were observed in mitochondria in cardiac muscle cells, neutrophil bone marrow cells and to a lesser extent (0-9%) in skeletal muscle cells. Membrane-bound vacuoles were seen in neutrophil bone marrow cells. Intramuscular fat droplets were increased in type I skeletal muscle fibres. An affected patient had intermittent lactic acidemia, borderline low plasma carnitine, the latter decreasing during periods of illness, and low muscle carnitine (27% pretreatment; 35-40% posttreatment). While on treatment with oral carnitine he had less weakness and no cardiac complaints, but his neutropenia was not affected. Respiratory chain abnormalities were observed in this patient's isolated skeletal muscle mitochondria. These were: (1) diminished concentrations of cytochromes c1 + c, b and aa3 to 29, 47 and 64% of the averaged controls, and (2) a lowered P:0 ratio for oxidation of ascorbate + TMPD, with diminished uncoupler stimulated Mg2+-ATPase activity. Muscle AMP deaminase was deficient (5 resp. 17%). Only one previous report (Neustein et al. 1979) on X-linked mitochondrial cardiomyopathy exists, which probably refers to the same entity. Biochemical studies and haematological abnormalities (neutropenia) are reported for the first time.
 ...
PMID:An X-linked mitochondrial disease affecting cardiac muscle, skeletal muscle and neutrophil leucocytes. 614 97