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 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

Acute volume expansion, an increase in sodium intake and a restraint on sodium excretion endow the plasma with the capacity to cause a natriuresis, to inhibit sodium transport and to stimulate vascular reactivity. One natriuretic substance, the atrial natriuretic peptide, has been identified. Cytochemical techniques can detect the presence of a Na-K ATPase inhibitor in the plasma of normal man and the rat, the concentration of which is controlled by salt intake. The substance responsible appears to originate in the hypothalamus. The plasma concentration of the cytochemically detectable Na-K ATPase inhibitor is substantially raised in the plasma of patients with essential hypertension, of the spontaneously hypertensive rat and of the Milan hypertensive rat. An hypothesis is put forward that links salt intake, a genetic renal lesion, the endogenous Na-K ATPase inhibitor, the atrial natriuretic peptide, and the substance responsible for vascular reactivity, with the rise in arterial pressure in hereditary forms of hypertension.
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PMID:[Cytochemical demonstration of an endogenous inhibitor of Na-K ATPase and its relationship to familial arterial hypertension]. 303 98

In this chapter are outlined the many factors involved in the regulation of sodium and volume homeostasis in normal human pregnancy and their interrelationships. New developments concerning the role of sodium/potassium ATPase, atrial natriuretic peptide, arginine vasopressin and angiotensin II as regulatory forces are outlined, together with a review of earlier work. Abnormalities found in women with, or destined for, PAH are described and their significance is discussed.
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PMID:Volume homeostasis in normal and hypertensive human pregnancy. 333 Apr 88

Acute volume expansion endows the plasma with the capacity to cause a natriuresis, to inhibit Na-K-ATPase and to stimulate vascular reactivity. These changes are due to a change in the concentration of two or more substances in the plasma. Atrial natriuretic peptides do not inhibit Na-K-ATPase and they decrease vascular reactivity. The search for the Na-K-ATPase inhibitor has been hampered by the lack of specificity of most assays which demonstrate the presence of many irrelevant Na-K-ATPase inhibitors. Cytochemical bioassays, however, appear to have a certain selectivity. They disclose the presence of a Na-K-ATPase inhibitor in the plasma, the concentration of which is controlled by salt intake but the only known substance so far tested, which these bioassays will detect, is ouabain. The hypothalamus contains the highest concentration of the cytochemically bioassayable inhibitory material and its content is also controlled by salt intake. The substance responsible for the cytochemically bioassayable inhibitory activity in the plasma and the hypothalamus share the same physico-chemical properties and on extraction appear in the same fraction. It is possible therefore, that the Na-K-ATPase inhibitor which is detectable by the cytochemical assays in the plasma and hypothalamus is the same. The concentration of cytochemically bioassayable Na-K-ATPase inhibitory activity is raised in the plasma of patients with essential hypertension, the SHR rat and the Milan hypertensive rat, as is the concentration of atrial natriuretic peptide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The endogenous cytochemically assayable Na-K-ATPase inhibitor and its relation to hypertension. 359 1

The aims of treatment of chronic heart failure are to improve the symptoms and the quality of life, reduce mortality and prevent left ventricular dysfunction. Before the first symptom occurs, neurohormonal activation takes place (increased catecholamines and atrial natriuretic peptide levels). Diuretics improve symptoms and are irreplaceable for the elimination of salt and water overload. Loop diuretics are used more often than the thiazides. Their deleterious effects on electrolyte balance are well known. The fact that they activate the renin angiotensin system is a more recent acquisition; the increase in plasma renin activity is a poor prognostic factor. Diuretics potentialize the vasodilator effect of angiotensin converting enzyme inhibitors which inhibit the neurohumoral activation induced by the diuretics. This therapeutic association is very logical, effective and allows reduction in the dosage of the diuretic. To date, there are no large scale controlled studies of the effects of diuretics on mortality. Spironolactone corrects hypokalaemia and hypomagnesaemia induced by loop diuretics. Moreover, it has been shown experimentally in renovascular hypertension and in hyperaldosteronism, that this molecule can prevent myocardial fibrosis, a factor which leads to ventricular dysfunction. The RALES study will analyse the effect of associating spironolactone to diuretic and ACE inhibitor therapy on the mortality of patients in NYHA classes III-IV. The value of digitalis in heart failure patients with sinus rhythm is a classical controversy. Digitalis has a positive inotropic effect (inhibition of NaK-dependent ATPase). More recently, a favourable neurohormonal effect has been reported; digitalis decreases the activation of the sympathetic and renin-angiotensin systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Classic treatment of chronic heart insufficiency. What if new?]. 748 8

In this work we analyze the renal and systemic factors involved in the sodium retention in two conditions: in extracellular volume depletion and in edema forming states, particularly liver cirrhosis with ascitis. In this paper we accept that the volume loss of body fluids stimulates the "effective arterial blood volume" (VAE). This term results from a decrease in the arterial blood volume secondary to a fall in cardiac output or a peripheral arterial vasodilatation. The reduction in the VAE stimulates: the high pressure baroreceptors (carotid sinus and aortic arch); the intrarrenal mechanisms, such as the yuxtaglomerular apparatus and the renin angiotensin aldosterone system; the sympathetic adrenergic system; the non osmotic release of antidiuretic hormone; prostaglandins (PGE1, Tromboxane) and endothelin; and inhibits the atrial natriuretic peptide. We also describe the sodium transport mechanisms along the nephron during physiological conditions and after volume depletion, and in edema formation states, specially hepatic cirrhosis with ascitis. We speculate that the intrarenal mechanisms are more important and persistent than the systemic mechanisms. It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. The clonation and structural characterization of the different sodium transports may help us to establish, more precisely, the intracellular tubular mechanisms responsible for the tendency of the body to retain sodium. The amount of information generated in the future may help us to demonstrate, with more precision, the mechanisms responsible for the sodium retention and excretion in normal and pathological conditions, particularly the edema forming states such as cardiac failure, nephrotic syndrome and hepatic cirrhosis with ascitis.
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PMID:[Renal and extra-renal mechanisms of sodium and water retention in cirrhosis with ascites]. 777 18

Prior studies indicate that the natriuretic effects of atrial natriuretic peptide (ANP) are due, in part, to an inhibition of the passive movement of sodium ions from tubular lumen through apical cation channels into renal tubular epithelium. The present work demonstrates that ANP also exerts a potent inhibitory effect on the active pumping of sodium ions by renal tubular sodium and potassium-activated adenosine triphosphatase (Na, K-ATPase). This action of ANP is relatively long lasting, is due to a change in enzyme Vmax and is specific for ouabain-sensitive activity. Enzyme modulation occurs with an EC50 for ANP of 0.1 nM, is independent of intracellular [Na+] and is associated with an increase in tissue cyclic GMP (cGMP), but not cyclic AMP (cAMP). Modulation of Na, K-ATPase by ANP is mimicked by 8-bromo-cGMP and okadaic acid (OA) and is blocked by KT 5823, a selective inhibitor of cGMP-dependent protein kinase (PKG), but not by KT 5720, a selective inhibitor of cyclic AMP-dependent protein kinase (PKA), which suggests that the action of ANP on the sodium pump involves cGMP-mediated changes in protein phosphorylation. Regulation of renal Na, K-ATPase activity also occurs with nitric oxide-generating compounds, such as nitroglycerin and sodium nitroprusside (SNP). However, the ability of ANP to modulate Na, K-ATPase does not appear to involve this latter pathway because the effects of ANP on the sodium pump cannot be blocked by either N omega-nitro-L-arginine, an inhibitor of NO synthase, or hemoglobin, which blocks NO through binding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide modulates sodium and potassium-activated adenosine triphosphatase through a mechanism involving cyclic GMP and cyclic GMP-dependent protein kinase. 789 13

Human urine and plasma extracts contain a material that inhibits the enzyme Na+,K(+)-ATPase (the endogenous sodium pump) and produces natriuresis in the bioassay animal. This endogenous sodium pump inhibitor(s), also known as digitalis-like factor, is thought to be involved in sodium and extracellular fluid volume homeostasis. Increased urine and plasma sodium pump inhibiting activity have been reported in patients with cirrhosis and sodium retention. The aim of the study was to assess the renal response to i.v. administration (0.2 ml/min per kg bw for 10 min) of a human urine extract containing sodium pump inhibiting activity (28.5 nmol equivalent ouabain/ml) in eight conscious rats with cirrhosis and ascites and eight control rats. Baseline urinary excretion of Na+,K(+)-ATPase inhibiting activity was significantly higher in cirrhotic rats with ascites than in control rats (235 +/- 40 vs 91 +/- 16; p < 0.01). Human urine extract induced a significant (p < 0.05) increase in glomerular filtration rate in control (3.2 +/- 0.4 to 4.2 +/- 0.5 ml/min) and cirrhotic rats (3.0 +/- 0.3 to 4.0 +/- 0.5 ml/min). In control rats it also increased urinary sodium excretion (1.47 +/- 0.22 to 2.43 +/- 0.5 microEq/min, p < 0.01) and fractional sodium excretion (0.29 +/- 0.01 to 0.43 +/- 0.04%, p < 0.025). In contrast, in cirrhotic rats with ascites neither sodium excretion nor fractional sodium excretion was significantly affected. No changes were observed in plasma aldosterone and atrial natriuretic peptide concentrations in either group. These data suggest that in cirrhosis there is a renal resistance to the natriuretic effect of endogenous sodium pump inhibitor(s).
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PMID:Blunted natriuretic response to human urine extracts with Na+,K(+)-ATPase inhibiting activity in experimental cirrhosis. 807 45

In order to elucidate whether the secretion of atrial natriuretic peptide (ANP) is correlated to the release of calcium (Ca) from the atrial specific granules (ASG), it is necessary to explore whether the ASG contain highly concentrated Ca and how the high Ca is maintained in the ASG. The present study was designed to determine Ca in the ASG with the quantitative electron microscope X-ray microanalysis and Ca(2+)-ATPase with electron microscopic (EM) cytochemical technique. The ultrathin cryosections of rapid frozen fresh rat auricles were used for measuring Ca concentration with a JEM-1200EX electron microscope equipped with a Link AN 10,000 energy dispersive X-ray spectroscope. The measurement showed that the Ca concentration in the ASG was quite high, being 81 +/- 15 mmol/kg (n = 10), comparable with that found in the sarcoplasmic reticulum. With the Ca(2+)-ATPase EM cytochemical technique, the reaction products proved to be deposited on the membrane of the ASG. It was postulated that the Ca(2+)-ATPase on the membrane of ASG pumped Ca2+ out of the cytosol into the ASG and thus maintained a high Ca concentration inside the ASG. Therefore, the ASG might be considered to be a Ca store in atrial cardiocytes.
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PMID:[Atrial specific granules are an intracellular calcium store]. 808 66

The authors have previously shown that atrial natriuretic peptide (ANP) mediates its cellular effects in part by changes in Ca2+ homeostasis in kidney cortex and that Ca2+ + Mg2+ ATPase is linked to ANP receptors, being reciprocally modulated by the guanylate cyclase system. The present study was designed to examine the status of this coupling in diabetes-induced congestive heart failure and the effect of its alterations on the functional integrity of the renal cell. Ca2+ + Mg2+ ATPase and guanylate cyclase were tested in hypertensive-diabetic rats (D + H), which develop congestive heart failure (CHF) at ten weeks following streptozotocin (65 mg/kg) injection and abdominal aortic constriction. The ATPase activity was measured by the release of 32P from [gamma-32P]ATP in the medium. While the guanylate cyclase activity was decreased very rapidly in the hypertensive-diabetic group, the sensitivity of the Ca2+ pump to ANP was increased at an early stage (three weeks) and decreased at a late stage (ten weeks) of CHF. The authors conclude that a defect in coupling between the Ca2+ pump and the ANP-receptor system as observed in the D + H group may contribute to the development of nephropathy and CHF.
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PMID:Renal Ca2+ + Mg2+ ATPase in congestive heart failure due to diabetes. 810 29


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