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

---

Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An initial characterization of the lenticular ionic permeabilities of the isolated Sprague-Dawley rat lens utilizing short-circuiting techniques was carried out to provide the basis for further studies of mechanisms underlying cataractogenesis associated with salt-sensitive genetic hypertension in the rat. Both active and passive Na+ and K+ transport were evaluated by varying ionic concentrations in the bathing solutions facing the anterior and posterior sides of the lens, as well as by the addition of BaCl2 and ouabain. In general, the ionic permeabilities and transport properties of the rat lens are qualitatively similar to those previously described in other species. Ionic replacement studies showed the presence of Na+ and K+ channels at both surfaces of the lens, with the anterior side K+ conductance being larger than the posterior. In contrast, Na+ conductance was similar at both lens surfaces. The effects of ouabain confirmed the presence of the Na(+)-K(+)-ATPase at the lens epithelium, while the effects of serial addition of BaCl2 and ouabain suggested that the contribution of K+ diffusion to the short-circuit current may be considerably greater than the electrogenic component of the Na(+)-K+ pump.
...
PMID:Characterization of active and passive Na+ and K+ transport in normal rat lens by the short-circuiting technique. 131 40

1. Vascular contractions induced by K(+)-free solution and relaxation responses following the return of K+ to the organ bath were studied in mesenteric arterial rings from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) with particular focus on the role of vascular adrenergic nerve-endings and endothelium. 2. In endothelium-denuded rings the omission of K+ from the incubation medium resulted in gradual contractions, the rate of which was slower in SHR than WKY. Nifedipine (1 microM) inhibited the contractions more effectively in SHR than WKY. 3. Adrenergic denervation in vitro with 6-hydroxydopamine reduced the contractions induced by the K(+)-free medium in endothelium-denuded rings. The remaining contractions after denervation were markedly greater in SHR than WKY. 4. The presence of intact vascular endothelium attenuated the K(+)-free contractions in both strains, the attenuation being smaller in SHR than WKY. NG-nitro-L-arginine methyl ester (L-NAME, 0.1 mM) and methylene blue (10 microM), but not indomethacin (10 microM), abolished the attenuating effect of endothelium on the K(+)-free contractions. L-Arginine (1 mM) reversed the effect of L-NAME in WKY but not in SHR. 5. The re-addition of K+ after full K(+)-free contractions dose-dependently relaxed the rings. The rate of this K(+)-induced relaxation was significantly slower in SHR than WKY at all K+ concentrations (0.1-5.9 mM) studied, whether the endothelium or functioning adrenergic nerve-endings were present or not. Ouabain (1 mM) totally inhibited the K+ relaxation in SHR but only partially in WKY.6. Vascular smooth muscle contractions induced by high concentrations of potassium were comparable between the strains. The EC50 for noradrenaline-induced contractions was lower in SHR than WKY, but the maximal forces did not differ significantly.7. In conclusion, the contractile response in K+-free solution more clearly differentiates vascular rings from SHR and WKY than the responses induced by the classical contractile agents noradrenaline and high concentrations of potassium. The depressant effect of the presence of intact endothelium on the K+-free contractions, which was smaller in SHR than WKY, is mediated via the endothelium-derived relaxing factor. Neurotransmitter release from vascular adrenergic nerve-endings participates less in the K+-free contractile response in SHR than WKY. Moreover, the contractile response is more dependent on calcium entry through nifedipine-sensitive calcium channels in SHR than WKY. The greater K+-free contractions of denervated endothelium-denuded rings and the reduced K+ relaxation rate in SHR when compared to WKY suggest increased cell membrane permeability and decreased activity of vascular Na+, K+-ATPase, respectively, in this type of genetic hypertension.
...
PMID:Contractions induced by potassium-free solution and potassium relaxation in vascular smooth muscle of hypertensive and normotensive rats. 150 24

Circulating digitalis-like compounds have been found elevated in some experimental sodium--and volume--dependent hypertensions, as well as in human essential hypertension. As few studies have been undertaken to assess their enhancement in the genetic hypertension of Okamoto (SHR) we have investigated their presence in plasma using 4 criteria: their apparent immunoreactivity with antidigoxin antibodies, their competition with tritiated ouabain binding to the sodium pump of human red blood cells,-their ability to inhibit the Na+, K+ ATPase activity of rat kidney membranes, and the Na+ fluxes from rat red blood cells. When compared to ordinary Wistar (W) and Wistar Kyoto rats (WKY), SHR exhibited a markedly enhanced apparent immunoreactivity with antidigoxin-antibodies (138 +/- 8; 59 +/- 3; 61 +/- 4 pg/ml, n = 15, 6 et 15, p less than 0.001, and p less than 0.001 respectively). The inhibition of ouabain binding by plasma extracts of the three strains did not differ (10.3 +/- 1.6, 9.9 +/- 1.7 and 12.9 +/- 1.4 ng/ml, n = 9, 18 and 14 respectively). When compared to WKY, SHR plasma extracts inhibited the renal Na+, K+ ATPase activity (75.6 +/- 2.6 vs 89.3 +/- 2.4 mumoles Pi . mg-1 . h-1, n = 11 and 10, p less than 0.01, respectively). When incubated in SHR plasma for one hour, net sodium effluxes from Wistar erythrocytes were inhibited compared to that measured in the presence of W or WKY plasma: (5.91 +/- 0.20 vs 7.68 +/- 0.25 and 7.52 +/- 0.15 mmol/l cells, n = 5, 3 and 5, p less than 0.001, and p less than 0.001 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Genetic hypertension in the SHR rat and circulating digitalis compounds]. 282 51

Male spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY) were subjected to swimming training 6 times/wk, commencing at 4 wk of age, to determine whether this type of endurance exercise might alter contractile proteins and cardiac function in young adult SHR. The total duration of exercise was 190 h. Myofibrillar adenosinetriphosphatase (ATPase) activity was assayed at various free [Ca2+] ranging from 10(-7) to 10(-5) M. Ca2+-stimulated ATPase activity of actomyosin and purified myosin was determined at various Ca2+ concentrations both in the low and high ionic strength buffers. Actin-activated myosin ATPase activity of purified myosin was assayed at several concentrations of actin purified from rabbit skeletal muscle. Under all these conditions the contractile protein ATPase activity was comparable between trained and untrained WKY and SHR. Analysis of myosin isoenzymes on pyrophosphate gels showed a single band corresponding to V1 isoenzyme, and there were no differences between swimming-trained and nontrained WKY and SHR. Ventricular performance was assessed by measuring cardiac output and stroke volume after rapid intravenous volume overloading. Both cardiac index and stroke index were comparable in nontrained WKY and SHR but were significantly increased in the trained groups compared with their respective nontrained controls. These results suggest that myosin ATPase activity and distribution of myosin isoenzymes are not altered in the moderately hypertrophied left ventricle whether the hypertrophy is due to genetic hypertension (SHR) or to exercise training (trained WKY). Moreover, the data indicate that SHR, despite the persistence of a pressure overload, undergo similar increases in left ventricular mass and peak cardiac index after training, as do normotensive WKY.
...
PMID:Effect of swimming training on cardiac function and myosin ATPase activity in SHR. 293 19

The ability of plasma extracts to inhibit Na+-K+ ATPase in vitro (P.I.A.) was tested in 20 normotensives, 10 without (F-) and 10 with (F+) familial hypertension, in 20 borderlines (BL) and in 21 essential hypertensives (EH). In these subjects we also measured intralymphocytic sodium (ILSC) and potassium (ILKC) content, P.R.A. urinary aldosterone and Na+(Na+u), and blood pressure. P.I.A. of EH, BL and F+ subjects was significantly higher than that of F-. 60% of EH and BL and 40% of F+ had P.I.A. values greater than the highest found in F-. P.I.A. was significantly related to mean blood pressure (r = 0.63), to ILSC (r = 0.56), to ILKC (r = -0.56), to ILSC/ILKC ratio (r = 0.71) and to Na+u (r = 0.39) but not to P.R.A. or aldosterone. These data demonstrate that plasma extracts from young subjects prone to hypertension may inhibit sodium pump and that this inhibitor may affect blood pressure by altering the Na+/K+ intracellular ratio.
...
PMID:Plasma Na+-K+ ATPase inhibitory activity in normal and hypertensive subjects: relationship to intracellular electrolytes and blood pressure. 299 Jul 69

Sodium-pump ATPase is known to be a cell membrane enzyme being responsible for vectorial transport of Na+ against electrochemical gradient across the plasma membranes of most cell types. In smooth muscles, this Na+-pump ATPase activity is notoriously low and its measurement is complicated by remarkably high level of the basal ATPase activities. In this communication, the properties of ouabain-sensitive, potassium-activated p-nitrophenyl phosphatase (pNPPase) activity which is a partial reaction of the Na+-pump are reported and compared in plasma membrane enriched fractions of mesenteric arteries from hypertensive and normotensive rats. The pNPPase activity of isolated plasma membrane vesicles from this vascular muscle is optimally stimulated by low concentrations of KCl (5-25 mM) at pH 7.8. Ouabain at 1.0 mM inhibits up to 75% of the K+-activated pNPPase activity under the optimal assay condition. Osmotic shock of the plasma membrane vesicles resulted in about 30% enhancement of the ouabain-sensitive K+-pNPPase activity compared to the control values. Although apparent difference was observed in this enzyme activity using similar preparations obtained from rats of different strains, the relative enhancement of such ouabain-sensitive K+-pNPPase activities by osmotic shock was not significantly different between vascular membrane fractions from the spontaneously hypertensive rats and the Wistar-Kyoto normotensive rats. Our results suggest that the intrinsic Na+-pump activity of small blood vessels in genetic hypertension in rats is not altered and the isolation procedure does not have differential effect on the orientation of plasma membrane vesicles in fractions obtained from hypertensive and normotensive rats.
...
PMID:On the ouabain-sensitive potassium activated p-nitrophenyl phosphatase activity of vascular muscle plasma membranes. 609 31

In this review, postulated passive and active fluxes of sodium, potassium, and calcium across the sarcolemma of the normal vascular smooth muscle cell are first summarized. Some practical problems encountered in their measurement are also mentioned. The review then considers how these fluxes appear to be altered in various forms of hypertension in animals and humans. Emphasis is given to abnormal fluxes of sodium and potassium due to altered sodium pump activity and permeability. Increasing evidence indicates that sodium retention due to increased sodium intake or decreased sodium excretion causes hypertension by releasing a humoral pressor substance from brain. This substance, which may be the putative natriuretic hormone, inhibits Na+, K+-ATPase and sodium pump activities in blood vessels and heart, thereby increasing contractile activity. In the genetic models of hypertension, the primary defect appears to be increased permeability of the vascular smooth muscle cell wall to sodium; pump activity increases to compensate for the increased inward leak of sodium. This may also be the case in patients with heritable essential hypertension. The possible consequences of super-imposing the sodium pump inhibitor on the primary defect are also considered. This may occur when animals with genetic hypertension or patients with heritable essential hypertension retain sodium subsequent to increased sodium intake and/or decreased ability to excrete sodium. Such superimposition should raise intracellular sodium concentration to high levels since now the pump would not fully compensate for the increased inward leak of sodium.
...
PMID:Abnormalities of membrane transport in hypertension. 636 Aug 83

Microsomal fractions were isolated from the smooth muscle of gastric fundus, vasa deferentia and mesenteric arteries of rats made hypertensive by deoxycorticosterone-salt treatment. Several enzymatic activities, Ca2+ binding and ATP-dependent Ca2+ accumulation of the microsomal fractions from these hypertensive rats were compared with those from the control of rats which remained normotensive under similar treatment. Altered membrane properties were observed in microsomal fractions isolated from vascular smooth muscle but not in those isolated from non-vascular smooth muscles in this form of experimental hypertension. These alterations included decreased Mg2+ ATPase activity, enhanced alkaline phosphatase activity, decreased Ca2+ binding in the absence of ATP and decreased ATP-dependent Ca2+ accumulation. This result is in contrast to our previous findings that decreased ATP-dependent Ca2+ accumulation was observed in microsomal fraction isolated from non-vascular smooth muscles of rats with genetic hypertension. The present study, together with our previous findings, support the contention that altered Ca2+ handling by vascular smooth muscle is associated with the pathogenesis of hypertension, whereas altered Ca2+ handling by non-vascular smooth muscles previously observed in spontaneous hypertension may be associated with genetic factors not related to hypertension.
...
PMID:Membrane abnormalities occur in vascular smooth muscle but not in non-vascular smooth muscle from rats with deoxycorticosterone-salt induced hypertension. 668 Oct 43

Transport features of calcium in red cells of rats with spontaneous genetic hypertension (SHR) have been studied. It is shown that in the presence of calmodulin the rate of calcium accumulation by the inside-out vesicles of SHR red cell membranes is roughly twice less than in the control normotensive rats. It is suggested that upset interrelationship between calmodulin and Mg-Ca-ATPase of plasma membrane may be the cause of increase of intracellular calcium recorded in a number of tissues in primary hypertension.
...
PMID:[Calcium transport in the erythrocytes of rats with spontaneous hypertension: characteristics of the effect of calmodulin]. 710 56

Plasma digitalis-like substance and altered function of arterial Na+,K(+)-ATPase have both been linked with elevated blood pressure, but the influence of antihypertensive therapy on these factors remains unknown. Therefore, we treated spontaneously hypertensive rats and normotensive Wistar-Kyoto rats with the angiotensin-converting enzyme inhibitor quinapril for 10 weeks. The therapy markedly reduced blood pressure and plasma digoxin immunoreactivity, and it normalized the elevated plasma Na+:K+ ratio in the hypertensive animals. Relaxations of endothelium-denuded denervated arterial rings induced by return of potassium to the organ bath upon precontractions elicited by potassium-free solution were used to evaluate the function of vascular Na+,K(+)-ATPase. The rate of potassium relaxation was faster in quinapril-treated hypertensive rats and in both Wistar-Kyoto groups than in the hypertensive controls. Potassium relaxation was also effectively inhibited by the Na+,K(+)-ATPase inhibitor ouabain in all groups. In addition, arterial contractions to potassium chloride and relaxations to nitroprusside were examined. The contractions to lower concentrations of potassium chloride (20 mM) were enhanced in untreated hypertensive rats when compared with the other groups, although the maximal responses were corresponding in all groups. The time to reach base-line tension after washout of potassium chloride (125 mM) and the relaxations to nitroprusside did not differ in the study groups. In conclusion, the present results showed that long-term angiotensin-converting enzyme inhibition in parallel reduced plasma digoxin-like factor, enhanced arterial potassium relaxation (probably reflecting enhanced function of Na+,K(+)-ATPase) and normalized plasma Na+:K+ ratio in this type of genetic hypertension.
...
PMID:Plasma digoxin immunoreactivity and arterial potassium relaxation after quinapril therapy in hypertensive rats. 747 73


1 2 3 Next >>

---