Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The ability of prostaglandins (PG) D2, E1, E2, F2 alpha and I2 (2.8 X 10(-11) to (2.8 X 10(-7) M) to modify Ca2+, Mg2+ and (Na+ + K+)-ATPase activities of rat heart sarcolemmal membrane fractions was examined. Administration of PGE2, PGF2 alpha, and PGI2 reduced basal (Na + + K+)-ATPase activity by up to 30, 80, and 80%, respectively. PGE1 and PGD2 were ineffective at any concentration. Neither Mg2+ -ATPase nor Ca2+ -ATPase was affected by PG treatment. Kinetic analysis revealed that the (Na+ + K+)-ATPase activity reducing ability of PGE2, PGF2 alpha and PGI2 was of a complex nature involving a reduction in Vmax and an elevation of the respective K values for either substrate or activator. These results demonstrate that some PG's are potent inhibitors of rat heart (Na+ + K+)-ATPase. These PG's produced varied inotropic influences on isolated heart preparations and it is uncertain whether their myocardial actions are dependent on enzyme inhibition.
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PMID:Effect of prostaglandins on rat heart sarcolemmal ATPases. 611 48

Experiments were made on the heart perfused according to Langendorf's method of adult Wistar and Okamoto-Aoki rats with hereditary arterial hypertension given the diets with varying content of polyunsaturated fatty acids (PUFA). It was demonstrated that under total heart ischemia, there was a maximal increase in the output of prostacycline and prostaglandin E (PGE) by the hearts of hypertensive rats given the diet enriched with linoleic acid. The rats given the PUFA deficient diet and the diet enriched with linoleic acid did not show any substantial changes in PG secretion by the ischemized heart. It was also disclosed that under normoxic perfusion, Na, K-ATPase activity in the heart of hypertensive rats was increased, being significantly inhibited during total heart ischemia. According to the authors, the differences in the changes in PG secretion and Na, K-ATPase activity might be related to a possible effect of lipid diet components and to variations in PUFA content in heart phospholipids.
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PMID:[Effects of a diet with various polyunsaturated fatty acid contents on the secretion of prostaglandins and ATPase activity in the rat myocardium in total ischemia]. 633 Oct 6

Although various prostaglandins have been shown to elicit an inotropic response in the rat heart, the subcellular basis responsible for this effect is unknown. The purpose of this study was to examine the influence of three prostaglandins with varying inotropic potencies on myofibrillar ATPase activity in the rat heart. PGF2 alpha, PGI2 and PGE2 were found to have no influence on basal or Ca2+-stimulated myofibrillar ATPase activity. In addition, no influence was observed on the sensitivity of myofibrillar ATPase activity to Ca2+. Alternative mechanisms to explain the inotropic effect are discussed.
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PMID:Lack of effect of prostaglandins on rat heart myofibrillar ATPase activity. 645 90

Pulmonary emboli may impair myocardial performance, causing declines in cardiac index (CI) and right and left ventricular stroke work (LVSW) because of mechanical events. We postulate that embolism also leads to the generation of a humoral factor(s) that may reduce cardiac contractility. Eleven mongrel dogs were infused with 0.5 gm/kg clot. Decreases in CI and LVSW were observed 1 hour after embolization. The stable metabolites of prostacyclin and thromboxane (Tx) A2--6-keto-PGF1 alpha and TxB2, respectively--increased within 30 minutes (P less than 0.005, P les than 0.001) and then decreased. These changes did not correlate with the declines in CI or LVSW. Plasma from embolized animals used to bathe an isolated rat papillary muscle reduced developed tension (Tpd) (P less than 0.001) and decreased calcium ATPase (Ca++-ATPase) activity of a myofibril preparation (P less than 0.001) obtained from rat cardiac muscle. The correlation between the reduction of TPd and myofibril Ca++-ATPase activity was 0.72 (P less than 0.001). The decline in Ca++-ATPase was also related to the decreases in CI (r = 0.59, P less than 0.001) and LVSW (r = 0.57, P less than 0.001). Five animals pretreated with indomethacin prior to embolization had no decrease in LVSW as compared with controls (P less than 0.001). Postembolism plasma did not depress papillary muscle Tpd and did not lower Ca++-ATPase activity of myofibrils. Anesthesia itself did not alter cardiopulmonary function. These results suggest that pulmonary emboli cause the release of a negative inotropic agent(s) into plasma that affects energy availability in the heart and reduces contractility. The production of this agent(s) is inhibited by indomethacin pretreatment.
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PMID:Circulating negative inotropic agent(s) following pulmonary embolism. 646 Oct 81

In porcine coronary artery endothelium-dependent relaxation to bradykinin is in part attributed to a chemically unidentified factor, termed endothelium-derived hyperpolarizing factor (EDHF). We hypothesize that arachidonic acid, acting through a cyclooxygenase-independent mechanism, is responsible for EDHF production. To define the relationship between EDHF production and arachidonic acid release, we investigated the role of phospholipase C in bradykinin-induced relaxation and prostaglandin I2 production (an index of arachidonic acid release) in porcine coronary artery. The phospholipase C inhibitor U73122 (1 mumol/L) abolished bradykinin-induced, nitric oxide-mediated relaxation but did not inhibit either bradykinin-induced, EDHF-mediated relaxation or prostaglandin I2 production. However, when given at a larger dose (20 mumol/L) U73122 abolished both bradykinin-induced, EDHF-mediated relaxation and prostaglandin I2 production. Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced. EDHF-mediated relaxation and prostaglandin I2 production. Although thapsigargin abolished bradykinin-induced prostaglandin I2 production, the basal production of prostaglandin I2 was enhanced and contraction of endothelium-intact rings was attenuated. These latter responses are most likely related to enhanced basal arachidonic acid release and associated EDHF production. These observations suggest that phospholipase C activation and increased intracellular calcium concentration are required for both bradykinin-induced arachidonic acid release and EDHF production in porcine coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of arachidonic acid release to porcine coronary artery relaxation. 755 31

Two proposed mechanisms of diabetic neuropathy are microvascular ischaemia and a reduction in Na,K-ATPase activity. We evaluated the effect of cilostazol, a drug that is both a potent phosphodiesterase inhibitor that normalizes nerve Na,K-AT-Pase and a vasodilator, on nerve blood flow (NBF) to determine whether it would improve experimental diabetic neuropathy. We examined whether epineurally applied cilostazol acted as a vasodilator on the peripheral nerve of normal and diabetic rats, and whether feeding the rats a cilostazol-supplemented diet could improve diabetic neuropathy. Cilostazol increased nerve blood flow (NBF) in a dose-dependent fashion with an EC50 of 10(-5.74) mol/l. Cilostazol also normalized NBF in experimental diabetic neuropathy with a 10(-4) mol/l local application on the sciatic nerve. In diabetic neuropathy, a cilostazol-supplemented diet improved both NBF and nerve conduction in a dose- and time-dependent fashion. Potential mechanisms of action of cilostazol on the nerve include its effect on NBF, Na, K-ATPase, and restoration of the thromboxane:prostacyclin ratio. Cilostazol may have potential in the treatment of diabetic neuropathy.
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PMID:Effect of cilostazol on experimental diabetic neuropathy in the rat. 758 76

We have investigated the relationship between cAMP and sodium,potassium-ATPase (Na+,K(+)-ATPase) activity in the sciatic nerves of rats treated with cilostazol, a potent phosphodiesterase inhibitor; iloprost, a stable prostacyclin analog; or (Bu)2cAMP, a cAMP analog, which increase cAMP content by different mechanisms. In in vivo studies, administration of cilostazol (20 mg/kg BW.day), iloprost (4 micrograms/kg BW.day), or (Bu)2cAMP (4 mg/kg BW.day) for 4 weeks restored decreased cAMP content and Na+,K(+)-ATPase activity in the sciatic nerves of diabetic rats and further improved motor nerve conduction velocities without alteration of myo-inositol contents. There was a positive correlation between cAMP contents and Na+,K(+)-ATPase activities in the sciatic nerves. In in vitro experiments, cAMP accumulation and Na+,K(+)-ATPase activity in the desheathed sciatic nerve blocks obtained from both normal and diabetic rats were significantly increased by incubation with cilostazol, iloprost, or (Bu)2cAMP. In addition, cAMP accumulation and Na+,K(+)-ATPase activities in endoneurial preparations incubated in both normal and high glucose buffer were also significantly increased by cilostazol, iloprost, and (Bu)2cAMP. These results strongly suggest that there is a close relationship between cAMP content and Na+,K(+)-ATPase activity in rat sciatic nerves. Therefore, cAMP content may play an important role in the development of diabetic neuropathy by modulating Na+,K(+)-ATPase activity in the peripheral nerves.
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PMID:Cyclic adenosine 3',5'-monophosphate enhances sodium, potassium-adenosine triphosphatase activity in the sciatic nerve of streptozotocin-induced diabetic rats. 767 91

In aspirin-treated platelets the thrombin-induced increase of cytosolic Ca2+ ([Ca2+]i) associated with the release from the intracellular stores is followed by a decrease to the baseline which is largely dependent on the re-uptake into the stores. This is shown by the further increase of [Ca2+]i upon inhibition of the endomembrane Ca(2+)-ATPase with thapsigargin. The re-uptake of Ca2+ into the stores is accelerated by sodium nitroprusside (SNP) or prostacyclin (PGI2). In all cases, after store depletion with thapsigargin the influx of external Ca2+ is maximal. After a thrombin-induced cycle of Ca(2+)-release re-uptake the stores are partly full: in these conditions the addition of external Ca2+ elicits a significant increment of [Ca2+]i and a further filling of the stores. Both are strongly reduced if Ca2+ addition is preceded by SNP or PGI2. Similar results are obtained also if (by supplementing and then cheleting Ca2+) the stores are as full as in native platelets at the moment of adding Ca2+. The thrombin-activated Ca2+ influx is reversed by hirudin. A PGI2- and SNP-sensitive Mn2+ influx is observed if Mn2+ is added in place of Ca2+. It is concluded that thrombin activates a cyclic nucleotide-sensitive Ca2+ (and Mn2+) influx pathway dependent on the occupancy of the thrombin receptor and independent of the filling state of the stores. In the absence of thrombin, thapsigargin releases Ca2+ relatively rapidly from a fraction of the stores; the remaining deposits are discharged much more slowly. This may indicate that platelets contain two distinct classes of agonist-sensitive stores. The addition of external Ca2+ (or Mn2+) at short or long incubation times with thapsigargin monitors the influx of Ca2+ activated by the depletion of one or both types of stores. The depletion of each type of store activates Ca2+ (Mn2+) influx. This type of cation influx is not inhibited by the cyclic nucleotides.
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PMID:Ca2+ influx in platelets: activation by thrombin and by the depletion of the stores. Effect of cyclic nucleotides. 798 Apr 23

To elucidate the effect of Beraprost, a stable prostaglandin (PG) I2 analogue, on airway smooth muscle functions and its mechanism of action, we studied canine bronchial segments under isometric conditions in vitro. Addition of PGI2 and its analogues dose-dependently relaxed bronchial smooth muscle precontracted with acetylcholine, with the rank order of potency being Beraprost (1) > or = Hoprost (0.65) > PGI2 (0.04), accompanied by the corresponding increase in intracellular cyclic AMP levels. The Beraprost- and PGI2-induced muscle relaxations were significantly inhibited by each of the PG antagonist diphloretin phosphate, the adenylate cyclase inhibitor SQ 22,536, and the Na(+)-K(+)-ATPase inhibitor ouabain. Beraprost and PGI2 at concentrations insufficient to cause muscle relaxation reduced the contractile responses to electrical field stimulation, whereas they were without effect on those to exogenous acetylcholine. These results suggest that Beraprost not only potently relaxes airway smooth muscle through cyclic AMP production and the subsequent stimulation of Na(+)-K(+)-ATPase but also reduces neurally mediated contraction by inhibiting the release of acetylcholine from the cholinergic nerve terminals.
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PMID:Relaxation and inhibition of contractile response to electrical field stimulation by Beraprost sodium in canine airway smooth muscle. 838 18

1. The effects of the Ca(2+)-ATPase inhibitor, thapsigargin, on the shear stress-dependent and on the agonist-stimulated release of endothelium-derived relaxing factor, i.e. nitric oxide (NO), and prostacyclin (PGI2) were studied in bovine and human cultured endothelial cells as well as in endothelium-intact arterial segments of the rabbit. 2. Preincubation with thapsigargin (1 microM for 10 min) had no effect on the shear stress-dependent release of NO from bovine aortic endothelial cells grown on beads, but abolished the release of NO induced by ADP, bradykinin, ionomycin or poly-L-lysine. Similarly, thapsigargin completely abrogated the agonist-stimulated PGI2 release from these cells, but had no effect on the shear stress-dependent release of PGI2. 3. The acetylcholine-induced release of NO from the luminally perfused thoracic aorta and femoral artery of the rabbit was suppressed by pretreatment with thapsigargin (1 microM). In contrast, thapsigargin did not affect the shear stress-dependent release of NO from the femoral artery. 4. Administration of thapsigargin to these vascular preparations or to cultured endothelial cells alone produced a substantial release of both NO and PGI2. This release declined towards previous values after washout of thapsigargin. 5. In human and bovine cultured endothelial cells, thapsigargin (1-1000 nM) caused a dose-dependent sustained rise in [Ca2+]i, an effect that was abolished in the absence of extracellular Ca2+. Stimulation of these cells with bradykinin, histamine, ADP or ionomycin after previous exposure to thapsigargin (30-1000 nM) no longer caused an increase in [Ca2+]i. of the release of these endothelial autacoids caused by shear stress or receptor-dependent and independent agonists.
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PMID:Selective inhibition of agonist-induced but not shear stress-dependent release of endothelial autacoids by thapsigargin. 842 99


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