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)

Red cell membrane Na(+)-K+ transport systems, renin-angiotensin-aldosterone system (RAAS) and atrial natriuretic factor (ANF) were studied in a group of 50 mild essential hypertensive patients (n = 25 for each group) age, sex and blood pressure matched. Na(+)-K+ ATPase and intracellular Na+ (Na+ i) were significantly different between the two groups (p less than 0.01). A slight difference was also seen for the Na(+)-K+ cotransport (p less than 0.05) as a likely consequence of the differences in the methodology of Na+ charge to study its efflux from the red cells in vitro. A negative correlation (r = -0.47, p less than 0.01) was observed between ANF and Na(+)-K+ cotransport suggesting an interrelationship of the two systems in the homeostasis in body fluid and electrolytes.
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PMID:[Erythrocyte cation transport in arterial hypertension: interrelation with the renin-angiotensin-aldosterone system and the atrial natriuretic factor]. 256 Sep 22

In this review, we first summarize the evidence which indicates that the inability of the kidney to excrete salt and water normally, particularly when combined with increased salt intake, is frequently associated with hypertension. We then concentrate on the link between sodium and water retention and hypertension. The increase in blood pressure probably results from the increase in volume rather than from the increase in salt. Recent evidence suggests that an increase in volume in the lesser circulation stimulates the release of a sodium pump inhibitor, probably the putative natriuretic hormone, from the hypothalamus. This agent appears to affect cardiac and vascular smooth muscle by suppressing Na+,K+-ATPase, and hence Na+-K+ pump activity in both muscle cells and adrenergic nerve terminals. The sodium pump inhibitor is a heat stable small molecule but its chemical structure is still unknown. It is clearly different from atrial natriuretic factor. We conclude the review with speculations on the possible role of renotropin and various growth and growth inhibitory factors in the vascular structural changes.
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PMID:The kidney in the pathogenesis of hypertension: the role of sodium. 258 44

We previously demonstrated that vascular smooth muscle cells possess a prominent Na+-K+-Cl- cotransport system that can be markedly stimulated by elevations in levels of intracellular cyclic guanosine 3',5'-monophosphate (cGMP). Since others have shown that atrial natriuretic factor (ANF) can bind to specific membrane receptors and can enhance cGMP levels in vascular smooth muscle cells, we asked whether ANF could also stimulate Na+-K+-Cl- cotransport in vascular smooth muscle cells. It was discovered that rat atriopeptin III stimulated Na+-K+-Cl- cotransport of vascular smooth muscle cells in a concentration-dependent manner. In contrast, rat atriopeptin III had no effect on two other sodium transport systems known to be present in vascular smooth muscle cells (i.e., Na+-H+ exchange and Na+-K+-adenosine triphosphatase (ATPase). These studies indicated that ANF selectively stimulates Na+-K+-Cl- cotransport of vascular smooth muscle cells. We then asked whether ANF-stimulated Na+-K+-Cl- cotransport was dependent upon the ability of ANF to enhance intracellular cGMP levels. When rat atriopeptin III-stimulated increases in cGMP were inhibited with the quinolinedione LY 83583, rat atriopeptin III could no longer stimulate Na+-K+-Cl- cotransport of vascular smooth muscle cells. Thus it appeared that the effects of ANF were dependent upon the ability of ANF to elevate intracellular cGMP levels. Finally, we asked whether ANF effects on Na+-K+-Cl- cotransport were related to the biological activity of ANF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of atrial natriuretic factor on Na+-K+-Cl- cotransport of vascular smooth muscle cells. 282 61

Atrial natriuretic peptides (ANPs) cause vasorelaxation, natriuresis and diuresis. Although the precise mechanism of action for these biological activities is not known, it has been established that ANPs can bind to specific membrane receptors and can cause an increase in intracellular cyclic GMP (cGMP) levels. In previously published studies we have probed the mechanism of action of ANP and have shown that one consequence of ANP receptor-mediated increases in cGMP in vascular smooth muscle cells (VSMC) is stimulation of Na/K/Cl cotransport. Although others have suggested that ANPs may affect Na/H exchange and/or Na/K adenosine triphosphatase (ATPase) activity in various cells and tissues, the effect of ANPs on these other Na transport systems in VSMC is not known. Furthermore, the biological relevance of ANP-stimulation of Na/K/Cl cotransport in VSMC has not been established. The goal of the present study was to investigate whether ANPs selectively stimulate Na/K/Cl cotransport in VSMC and to determine whether effects on cotransport parallel biological activity. We tested the effect of six ANPs on Na/K/Cl cotransport, and of one ANP on Na/H exchange and on Na/K ATPase activity. It was found that ANPs stimulated Na/K/Cl cotransport but had no effect on Na/H exchange or on Na/K ATPase activity in VSMC. Biological activity of the ANPs was assayed by measuring the potencies for producing vasorelaxation of aortic rings and for stimulating an increase in intracellular cGMP in VSMC. The rank orders observed for the two biological activities agreed with the rank order for stimulation of Na/K/Cl cotransport.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biologically active atrial natriuretic peptides selectively activate Na/K/Cl cotransport in vascular smooth muscle cells. 282 59

Tissue culture media from incubations of fragments of rat brain were collected and partially purified. These supernatants were effective in inhibiting the Na+-K+ pump as indicated by a 77% reduction of ouabain-sensitive 86Rb+ uptake into human erythrocytes. Release of the Na+-K+-ATPase inhibitor depended on the amount of tissue, the temperature, and the length of incubation. Atrial natriuretic peptide (ANP) injected intravenously, or included (10(-8) M) in the in vitro incubation of brain tissue, decreased the release of the Na+-K+-ATPase inhibitor by 74 and 42%, respectively. Control experiments using the neuropeptide arginine vasopressin showed no effect on release of the inhibitor. These studies indicate that ANP is capable of regulating the release from brain of a Na+-K+-ATPase inhibitor with similar chromatographic characteristics to the one previously obtained from extraction of bovine hypothalamus and raise the possibility that the two factors are interrelated in the regulation of fluid and electrolyte balance.
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PMID:Atrial natriuretic peptide regulates release of Na+-K+-ATPase inhibitor from rat brain. 283 11

Specific atrial natriuretic factor (ANF) analogues have been found to have inhibitory activity in vitro in a calmodulin-dependent, human red blood cell membrane Ca2+-adenosine triphosphatase (ATPase) model. Studied at 10(-8) to 10(-6) M concentrations, atriopeptin I (residues 127-147 of rat prepro-ANF sequence) and atriopeptin III (residues 127-150) progressively inhibited Ca2+-ATPase activity by up to 20% (p less than 0.001). This degree of inhibition was consistent with activities of other (calmodulin-independent) enzyme inhibitors in this model. Therefore, the C-terminal Phe-Arg-Tyr sequence (residues 148-150) is unnecessary for atriopeptin action on Ca2+-ATPase. Human and rat atrial peptides with amino acids 123-150 were inactive, indicating that the 123-126 sequence (Ser-Leu-Arg-Arg) must be cleaved to activate atriopeptins in this system. Human ANF fragment 129-150 also had no effect on Ca2+-ATPase, defining the importance of residues 127-128 (Ser-Ser) proximal to the disulfide bridge (joining 129 to 145). The addition of purified calmodulin to red blood cell membranes in the presence of inhibitory ANF did not restore Ca2+-ATPase activity to normal levels, indicating that the ANF effect on this enzyme is calmodulin-independent. Atriopeptin I and atriopeptin III had no effect on red blood cell Na+, K+-ATPase activity in vitro. Thus, the structure-activity relationships of ANF analogues in this novel human cell membrane model are highly specific. Although the inhibitory action of ANF analogues on Ca2+-ATPase, a calcium pump-associated enzyme, may be unique to the red blood cell, the calcium dependence of the gluconeogenic effects of ANF in the kidney would be supported by inhibition of this ATPase.
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PMID:Analogue-specific action in vitro of atrial natriuretic factor on human red blood cell Ca2+-ATPase activity. 284 69

Atrial natriuretic peptide (ANP) and Na+ pump inhibitor (digitalis-like substance, DLS) have both been proposed to participate in body sodium and water homeostasis. Plasma levels and ANP and DLS have been reported to be increased in physiological or pathological states characterized by volume expansion. In order to investigate possible mutual relationships, their concentrations were measured in parallel during acute volume expansion by injection of 25 ml/kg isotonic NaCl (A) or blood (B) in the conscious rat. ANP was measured by radioimmunoassay and DLS by inhibition of renal Na+, K+-ATPase activity and digoxin-like immunoreactivity (DLI). Five minutes after injection, plasma ANP increased to reach 700 pg/ml (A, n = 21) or 1,500 pg/ml (B, n = 5) but the ability of plasma extracts to inhibit the renal Na+, K+-ATPase activity was unchanged (16.6 +/- 2.5 vs 16.9 +/- 2.0 p. 100, A, n = 8 and 6). Digoxin-like immunoreactivity was slightly lowered after NaCl injection from (74.4 +/- 6.2 to 65.4 +/- 5.1 pg/ml, n = 21) and unchanged after blood injection (79.0 +/- 3.4 vs 81.2 +/- 5.0 pg/ml, n = 5). Plasma ANP concentrations then decreased and had returned to preinjection values before 30 (A) or 90 (B) minutes, whereas the capacity of plasma to inhibit the Na+, K+-ATPase tended to increase (25.9 +/- 4.7 p. 100 at 3 hours after injection, n = 12 compared to 17.6 +/- 1.6 p. 100, n = 20) and DLI remains stable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Variations in the plasma concentrations of atrial natriuretic factor and endogenous digitalis compounds during acute volume expansion in the conscious rat]. 284 69

The aim of this symposium on molecular biology in physiology was to introduce molecular biology to physiologists who had relatively little exposure to the new developments in this field, so that they can become conversant on this topic and contribute to the advancement of physiology by incorporating molecular biological approaches as a part of their research arsenal. After the discussion of the basic concepts, terminology, and methodology used in molecular biology, it was shown how these basic principles have been applied to the study of the genes encoding two membrane proteins that have important transport functions (band 3 and ATPase). The second half of the symposium consisted of papers on the state-of-the-art developments in the application of molecular biology to the studies of the atrial natriuretic factor and renin genes, adenylate cyclase-coupled adrenergic receptors, acetylcholine receptors and sodium channel, and long-term and short-term memories. The ultimate goal is that these examples will provide an impetus for the opening of new frontiers of research in physiology by taking advantage of the tools developed from recent advances in molecular biology.
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PMID:Molecular biology in physiology. 288 91

There appears to be two distinct natriuretic factors. One group, suspected since 1951 in overloaded dogs, had a low molecular weight: it belongs great affinity for ouabain, binds to digoxin antibodies and inhibits NA-K ATPase; this group seems heterogeneous in spite of the extraction of an amino glucosteroid-like substance from human urines. These factors are vasoconstrictor; the source is not still well known (hypothalamus ?). The atrial natriuretic factor (ANF) is a peptide about 20 to 25 amino acids and comes from a precursor of 152 amino acids, its synthesis was successful; secreted in the plasma from endocrine atrial granules, it causes striking natriuresis and diuresis and relaxes vascular and intestinal smooth muscle; it acts on guanylate cyclase but its renal mechanism of action is not well known; it constitutes an antagonist axe to ADH and RAA system. The relations between the two groups of natriuretic factors do not seem still very clear.
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PMID:[Natriuretic factors]. 295 21

Specific, high-affinity binding sites for atrial natriuretic factor (ANF) were identified and localized in the rat and guinea pig central nervous system (CNS), the cat brainstem, and the rat, guinea pig, cat and human spinal cord using quantitative autoradiographic techniques. The radioligands tested were rat 125I-ANF(1-28) in guinea pig, rat, cat and human tissues, human 125I-ANF in rat and human, and rat [3H]atriopeptin III in rat. All 3 radioligands labeled essentially the same structures in the brain and spinal cord of all species in which they were tested. In guinea pig very high concentrations of ANF binding sites were observed in the olfactory bulb, lateral olfactory tract and the granule cell layer of the cerebellum, high concentrations were observed in the fasciculus retroflexus, interpeduncular nucleus and subfornical organ. Moderate concentrations were observed in the nucleus accumbens, dorsomedial and suprachiasmatic hypothalamic nuclei, paraventricular thalamic nuclei, primary olfactory cortex and the subcommissural organ. High concentrations of ANF binding sites were also observed in the choroid plexus and the leptomeninges. Low concentrations were observed in the pineal gland. In the rat the same structures were labeled as in the guinea pig except that suprachiasmatic and dorsomedial hypothalamic nuclei, paraventricular thalamus and cerebellum were unlabeled. In the lower brainstem of the cat and all levels of the rat, guinea pig, cat and human spinal cord, the only site where specific binding was observed was in the pia/arachnoid. These findings suggest that ANF binding sites constitute several functional classes in the CNS as well as in a variety of other tissues. Outside the blood-brain barrier binding sites are prominent in glandular tissues implicated in the production of hormones involved in fluid and electrolyte balance, e.g. adrenal glomerulosa, neurohypophysis and subfornical organ, unstratified epithelia involved in ion gradient exchange, e.g. renal glomerulus, ciliary body, choroid plexus and pia mater; crossing the blood-brain barrier are sites in the anterior hypothalamus, e.g. organum vasculosum, regions of the brain parenchyma associated with angiotensin II binding sites, e.g. dorsomedial nucleus of hypothalamus, some of which may be occupied by brain rather than cardiac synthesized ANF, regions of brain lacking an obvious role in fluid and ion exchange or regulation, e.g. cerebellum, although association with K+,Na+-ATPase in guinea pig cerebellum may be a relevant clue and brain regions possibly implicated in an integrative and/or indirect regulatory role in fluid and electrolyte balance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Localization of specific binding sites for atrial natriuretic factor in the central nervous system of rat, guinea pig, cat and human. 295 51


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