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)

Ouabain has been reported to increase the secretion of ANP in vitro. In this study, we focused on whether this action is common in Na-K-ATPase inhibitors (ATPI) and whether ATPI simply increase the release of ANP or stimulate both its biosynthesis and release. The effects of ouabain and digoxin on secretion of ANP and accumulation of ANP mRNA were investigated in the rat cardiocyte superfusion system. Ouabain and digoxin increased the immunoreactive ANP (iANP) output into perfusate and accumulation of ANP mRNA significantly. These results suggest that ATPI may stimulate both ANP biosynthesis and release in vitro.
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PMID:Stimulation of atrial natriuretic peptide secretion and synthesis by Na-K-ATPase inhibitors. 185 Oct 7

Normal pregnancy is associated with a poorly understood loss of vascular responsiveness to the pressor effects of infused angiotensin II. Since cellular cation metabolism appears to be a critical determinant of basal vascular tone and vascular reactivity, we have evaluated platelet ionized calcium, erythrocyte sodium, calcium and magnesium levels, and erythrocyte Ca-ATPase and Na/K ATPase activity in 15 normal black pregnant women (37.5 +/- 0.6 weeks gestation) and 10 normal age-matched nonpregnant black women. Plasma levels of factors potentially affecting vascular reactivity (endoxin, renin activity (PRA), and atrial natriuretic peptide (ANP] were measured by RIA and peripheral vascular resistance by biolectrical impedance. Peripheral vascular resistance was almost twice as high (P less than .003) in the normal group as in the pregnant women. Intracellular calcium concentrations were not significantly different in erythrocytes or platelets of the two groups. Although erythrocyte membrane Ca-ATPase was similar, Na/K ATPase activity was significantly higher in the pregnant subjects than in the nonpregnant controls, and intracellular sodium was lower. All three measured plasma factors, ANP, endoxin and PRA, were significantly elevated in the pregnant women. Our results suggest that the decrease in peripheral vascular resistance seen in normal pregnancy is probably not the result of alterations in cellular cation concentrations and/or cell membrane pump activity. However, the significant correlation between vascular reactivity and circulating ANP indicates this potent vasodilator may play a role in the observed decrease in peripheral vascular resistance associated with pregnancy.
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PMID:Effects of normal pregnancy on cellular cation metabolism and peripheral vascular resistance. 215 37

Heart transplantation involves chronic effects due to denervation, rejection, and treatment of rejection. The chronically denervated dog heart provides a model for the effects of denervation alone. These hearts have been shown to contain intrinsic neurons with VIP and NPY as possible neurotransmitters. Myocardial tissue noradrenaline concentration falls to very low levels after degeneration of postganglionic sympathetic neurons, but dopamine remains in near-normal concentration and is probably synthesized extraneuronally. ANP is present and released normally; however, the natriuretic response to atrial distension is blunted, suggesting that this response is mainly due to a reflex mechanism. Chronically denervated myocardial tissue exhibits increased oxygen consumption in vitro and increased Na-K, ATPase activity but has normal tissue levels of ATP and creatine phosphate. Glucose oxidation is inhibited in vivo, associated with increased levels of fructose-6-phosphate but normal glucose-6-phosphate, suggesting inhibition of phosphofructokinase activity. However, the enzyme protein concentration of phosphofructokinase, as judged by maximal in vitro activity, is normal. Maximal in vitro activities of succinate dehydrogenase, cytochrome oxidase, monoamine oxidase, calcium-dependent ATPase, and glyceraldehyde-3-dehydrogenase are also normal. From these findings, we would predict that patients with transplanted hearts are likely to show myocardial metabolic inefficiency.
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PMID:Cellular abnormalities in chronically denervated myocardium. Implications for the transplanted heart. 253 6

The natriuretic properties of two small molecular weight endogenous compounds are reviewed. One may originate from the hypothalamus (natriuretic factor-NF) and the other from the cardiac atria (atrial natriuretic peptide-ANP). Differences in the intrarenal mechanisms of action of NF and ANP should be anticipated in view of the fundamentally different cellular effects of NF and ANP. NF is an inhibitor of (NaK) ATPase and inhibits active sodium transport across the isolated frog skin or toad bladder while ANP has no effect on NaK ATPase and sodium transport in vitro across the isolated anuran membrane. NF may have vasoconstrictive properties. In contrast ANP has vasorelaxing properties in some vascular beds and decreases blood pressure. Both compounds are diuretic, natriuretic and phosphaturic in intact kidneys and in kidneys with a decreased functional mass. Effects on potassium excretion are variable. For both, the increases in water and solute excretion are associated with several sites of action within the nephron. Whereas NF has little effect on glomerular filtration rate (GFR) and filtration fraction, ANP may induce impressive changes in kidney and in superficial nephron GFR, increasing the filtered load of water and solutes. ANP also increases filtration fraction changing, thereby, the peritubular physical forces of filtrate reabsorption. Both NF and ANP inhibit water and solute reabsorption in the proximal tubule. With NF, a direct tubular effect has been demonstrated in recollection micropuncture studies. In contrast, a direct epithelial effect has not been elicited with ANP in the proximal tubule.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natriuretic hormones: comparison of renal effects. 295 62

Human urine contains a small molecular weight natriuretic substance and similar material isolated from the kidney inhibits Na/K ATPase. Such action on blood vessels would cause contraction. Human urinary natriuretic material isolated from a Sephadex G-25 column contracted smooth muscle in the rat anococcygeus muscle. Known vasoactive substances could not explain the activity of the natriuretic fraction on the anococcygeus muscle. In subsequent studies the natriuretic fraction from the Sephadex G-25 column was run on a Sephadex G-10 column and natriuretic activity was found before the sodium was eluted. The same fractions inhibited Na/K ATPase but did not cause contraction of the anococcygeus muscle. The fractions which did cause contraction of the anococcygeus muscle were eluted long after the salts and these fractions did not inhibit Na/K ATPase and were not natriuretic. The postulated defect in sodium excretion in hypertensive patients might be related to their low kallikrein excretion. Since ANP stimulates increased kallikrein release in rats and does not inhibit Na/K ATPase, it is suggested that the natriuretic pathway via inhibition of renal Na/K ATPase is independent in the kidney of the kallikrein/kinin natriuretic pathway.
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PMID:Natriuretic and smooth muscle contracting activities isolated from human urine. 359 3

Ca2+ transport in kidney has gained considerable attention in the recent past. Our laboratory has been involved in understanding the regulatory mechanisms underlying Ca2+ transport in the kidney across the renal basolateral membrane. We have shown that ANP, a cardiac hormone, mediates its biological functions by acting on its receptors in the kidney basolateral membrane. Furthermore, it has been established that ANP receptors are coupled with Ca2+ ATPase, the enzyme that participates in the vectorial translocation of Ca2+ from the tubular lumen to the plasma. It is possible that a defect in the ANP-receptor-effector system in diabetes (under certain conditions such as hypertension) may be associated with abnormal Ca2+ homeostasis and the development of nephropathy. Accordingly, future studies are needed to establish this hypothesis.
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PMID:Renal handling of Ca2+ in diabetes. 781 51

1. ANP (atrial natriuretic peptides)- or ANP/ATP-stimulated guanylyl cyclase activities were compared in adult (2 month old) and neonatal (5-7 day old) rat lung membrane fractions. 2. The enzyme activities of both membranes depended on the incubation time and ATP concentration: although the activities of both membranes were similar after a short incubation time (4 min), those in adult membranes were lower than those of neonatal membranes after longer incubation times (10 and 30 min) or at lower concentrations of ATP. 3. ANP/ATP gamma S-stimulated guanylyl cyclase activities, which were much higher than ANP/ATP-stimulated activities, were similar in both membranes. 4. ATPase activity of adult membranes was higher than that of neonatal membranes, suggesting that hydrolysis of ATP leads to a decrease of ANP/ATP-guanylyl cyclase activity in adult membranes. Triton X-100 enhanced and diminished ANP/ATP-stimulated guanylyl cyclase activities of adult and neonatal membranes, respectively, and thereby abolished the adult/neonatal difference in the membrane response to ATP. 5. ANP-stimulated activities of both membranes were much more activated by pre-incubation with ATP gamma S than those induced by simultaneous addition of ATP gamma S. The former activities were decreased to levels of the latter by Triton X-100. The latter activities were not affected by Triton X-100. 6. The present results suggested that conformation of lung plasma membranes is related to activation of the ANP receptor/guanylyl cyclase system.
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PMID:Developmental changes in ANP-stimulated guanylyl cyclase activity enhanced by ATP in rat lung membrane fractions. 783 9

Cations like Mg2+ play an important role in the catalytic mechanism of F1-ATPases. In this study we applied ESR spectroscopy and used the ATP analog 2-azido-2',3'-(2,2,5,5-tetramethyl-3-pyrroline-1-oxyl-3-carboxylic acid ester)ATP (2-N3-SL-ATP) to investigate the effects of Mg2+ ions on the structure of the nucleotide binding sites of F1-ATPases from beef heart mitochondria (MF1) and from the thermophilic bacterium PS3 (TF1). The results demonstrated that Mg2+ ions not only influenced the binding of the nucleotide analogs to F1 but also altered the structure and geometry of the nucleotide binding sites. We observed that the dipolar interactions that are indicative of the close proximity of enzyme-bound 2-N3-SL-ANP (Vogel, P.D., Nett, J.H., Sauer, H.E., Schmadel, K., Cross, R.L., and Trommer, W.E. (1992) J. Biol. Chem. 267, 11982-11986) were only detectable in MF1-ATPase when the enzyme was preincubated with Mg2+ ions. In the absence of Mg2+, the enzyme exhibited ESR spectra indicative of spin label bound in at least two different environments (binding sites) with no dipolar interactions visible. TF1-ATPase did not exhibit clear dipolar interactions in the presence or absence of Mg2+. The ESR spectra of TF1 in the absence of Mg2+ indicated two different environments of the spin labels. Subsequent addition of Mg2+, however, led to exactly the same spectra as if the enzyme was incubated with the ions, indicating a rearrangement of the nucleotide binding sites. In summary, clear differences in the structures of the nucleotide binding sites of MF1 and TF1 in the presence or absence of Mg2+ were observed. Conformational differences between F1-bound spin-labeled nucleotides were also observed between TF1- and MF1-ATPases.
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PMID:Effects of magnesium ions on the relative conformation of nucleotide binding sites of F1-ATPases as studied by electron spin resonance spectroscopy. 802 34

The inner medullary collecting duct (IMCD) is the final arbiter of renal Na+ excretion, and Na+ transport in this segment is controlled by a wide variety of hormones and renal autacoids. This review examines the mechanisms of IMCD Na+ transport and its regulation using results obtained from micropuncture and microcatheterization studies in the intact animal, as well as data from isolated perfused tubules, freshly prepared cell suspensions, and cultured IMCD cells. Where appropriate, results from closely related tissues such as the cortical collecting duct and model urinary epithelia are examined. Na+ reabsorption in this segment occurs predominantly via apical amiloride-sensitive Na+ channels and basolateral Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase). Although there is some evidence for the activities of other transporters such as Na(+)-K(+)-2Cl- and Na-Cl cotransporters and Na+/H+ exchanger, their role in Na+ homeostasis remains undefined. Mineralocorticoids augment the activities of both apical Na+ channels and basolateral Na(+)-K(+)-ATPase by a variety of complex mechanisms. Prostaglandin E2 inhibits Na(+)-K(+)-ATPase and appears to mediate the actions of several peptide hormones, including endothelin, interleukin-1, and atrial natriuretic peptide [ANP-(31-67)]. Several peptides in the ANP family [ANP-(99-126), urodilatin, and brain natriuretic peptide] bind to guanylate cyclase-linked receptors, leading to inhibition of apical Na+ channel function. These mechanisms of regulation of IMCD Na+ transport likely play important roles in total body Na+ balance in health and disease.
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PMID:Hormonal regulation of inner medullary collecting duct sodium transport. 836 30

1. In mammalian plasma, many different inhibitors of Na+/K(+)-ATPase are present, but it is not clear whether their net effect on NA+/K(+)-ATPase activity changes during the regulation of electrolyte and fluid balance. We studied Na+/K(+)-ATPase inhibition by plasma extracts in conscious rats during short- and long-term body fluid regulation. 2. Male, adult, conscious, freely moving Wistar rats were subjected to one of the following protocols: (i) intracerebro-ventricular (i.c.v.) injections of angiotension II (AngII; 1, 10 and 100 ng), the AngII receptor antagonist losartan (1 microgram), atrial natriuretic peptide (ANP-III; 1 microgram) or isotonic saline (IS); (ii) intra-arterial (i.a.) injections of IS (6 or 10 mL), hypertonic saline (HS; 1.2% NaCl, 5 mL) or hypertonic plasma expander (HPS; 3.5% hetastarch in HS, 5 mL); or (iii) a low salt-high salt-low salt diet sequence (0.18/1.8/0.18% NaCl chow for 5 days each with controls receiving 0.18% NaCl on all days). Bodyweight, the intake of food and water, urine volume and Na+ concentration and weight of faeces were determined daily. Plasma samples were withdrawn repeatedly throughout the respective protocols, extracted on C18-reversed phase columns and assayed for their effect on the activity of different Na+/K(+)-ATPase preparations. 3. The inhibition of rat brain Na+/K(+)-ATPase by plasma extracts was not significantly changed by i.c.v. injection of AngII, losartan, ANP-III and IS within the observation period (30 min from respective stimuli). Similarly, no significant changes occurred after acute volume expansion by i.a. injection of IS or HS within 120 min; upon HPS, however, Na+/K(+)-ATPase inhibition was decreased by approximately 20% (P < 0.05), probably due to passive dilution. During the high-salt diet, fluid retention was effectively counteracted by an adaptive increase of urinary sodium excretion. Throughout the protocol, inhibition of pig brain Na+/K(+)-ATPase by plasma extracts did not differ significantly between groups. 4. It is concluded from these results that the short- or long-term control of body fluids in conscious rats is not associated with systematic changes in Na+/K(+)-ATPase inhibition by plasma factors.
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PMID:Circulating Na+/K+-ATPase inhibitors: effects of neuropeptides, volume expansion and salt loading in conscious rats. 907 84


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