Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.
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PMID:Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs. 13 55

The influence of isoenzyme pattern of myosin on cardiac energetics was investigated in a modified in situ heart-lung preparation in the rat. Chronic pressure load (spontaneous hypertension, aortic stenosis, Goldblatt hypertension), intermittent feeding, and swim-training elicited redistribution in the concentration of alpha chains of myosin ranging from 18 to 94%. The influence of isoenzyme pattern of myosin on cardiac energetics could be quantitatively assessed by extrapolation of the regression line of oxygen and substrate consumption related to tension time index. Fast myocardium with 100% alpha chains had an ATP and oxygen consumption which exceeded that of slow myocardium with 0% alpha chains by about 60%. This corresponds well to the state of activity of myofibrillar ATPase of fast myocardium which also exceeds that of slow myocardium by about 50%. Furthermore it could be shown that acute increase in the ATPase activity depends on the isoenzyme pattern of myosin. Under the influence of catecholamines the oxygen consumption related to tension time index increased by 30-40% in fast myocardium, whereby in a myocardium with 40% alpha chains no increase in oxygen consumption per unit tension time index was observed, when catecholamines were applied.
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PMID:Implications of myocardial transformation for cardiac energetics. 295 58

The properties of the Na/K pump and Na,K,Cl cotransporter were studied in vascular tissue of two-kidney Goldblatt hypertensive rats. These transport systems were measured as ouabain-sensitive and bumetanide-sensitive 86Rb/K uptake in aortic rings, left ventricular muscle and soleus skeletal muscle fibers of control and hypertensive Sprague-Dawley rats. A dramatic increment in Na/K pump activity was observed in intact aortic rings from the hypertensive group. The same was true for the Na,K,Cl cotransporter. The transport parameters related to the left ventricular muscle and soleus skeletal muscle were not significantly altered in the hypertensive rats. Measurements of the catalytic isoforms of the Na+, K(+)-ATPase in the aortic rings indicated that both isoforms (alpha 1 and alpha 2) were elevated in the same proportion in the hypertensive rats. The results also indicate that the endothelium plays an important role in both transport systems: in the absence of endothelium, a much lower 86Rb/K uptake was observed than in intact aortic rings, either from control or hypertensive vascular tissue. Nevertheless, when the 86Rb/K transport activity was measured in denuded aortic rings, a significantly higher ouabain and bumetanide sensitive 86Rb/K uptake was also observed in the hypertensive rats. These data also show no alteration in the endothelium of the hypertensive rats as compared to control animals. The presence of endothelium had a more striking effect on the alpha 2 catalytic isoform activity than on the alpha 1 isoform. We conclude that there is a significant increment in the Na/K pump and Na,K,Cl cotransporter in two kidney-Goldblatt hypertension, that is specific for vascular smooth muscle.
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PMID:Increased Na,K,Cl cotransporter and Na, K-ATPase activity of vascular tissue in two-kidney Goldblatt hypertension. 983 May 14