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Dissertations / Theses on the topic 'Peptide natriuretico atriale'

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Published: 21 February 2023
Last updated: 9 March 2023

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1

DELLA, CORTE Vittoriano. "RENAL SALT WASTING: UNA SINDROME DA INAPPROPRIATA SECREZIONE DI URODILATINA? UNO STUDIO PILOTA." Doctoral thesis, Università degli Studi di Palermo, 2022. https://hdl.handle.net/10447/554922.

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La Renal Salt Wasting Syndrome (RSW) è una sindrome clinica con caratteristiche di laboratorio che si sovrappongono completamente alla sindrome da secrezione inappropriata di ADH (SIADH). La differenza fondamentale tra le due sindromi risiede nel volume extracellulare (ECV), ridotto nella RSW e normale o leggermente aumentato nella SIADH. Le difficoltà nella diagnosi differenziale di questa sindrome e nella comprensione del preciso meccanismo patogenetico hanno contribuito a mettere in discussione l'esistenza stessa di RSW. Considerando le caratteristiche della RSW, è stato studiato il possibile ruolo dei peptidi natriuretici per spiegare la sua patogenesi come ANP e BNP, con risultati insoddisfacenti. Tuttavia, nessuno studio ha ancora indagato il possibile ruolo dell'urodilatina, un peptide appartenente alla famiglia dei peptidi natriuretici, che sembra avere un ruolo cruciale nella regolazione della sodiemia e del sodio urinario anche più dell'ANP. Abbiamo eseguito uno studio osservazionale retrospettivo, i pazienti sono stati divisi in 3 gruppi: un gruppo di pazienti senza iponatriemia e due gruppi di pazienti con iponatriemia, uno costituito da pazienti con RSW e l'altro costituito da pazienti con iponatriemia da altre cause. I pazienti con RSW mostrano livelli medi di urodilatina significativamente più elevati rispetto a entrambi i pazienti con (mediana 5,46 vs 0,57 ng/mL, p=0,006) o senza iponatriemia (mediana 5,46 vs 0,27 ng/mL, p<0,001). Livelli medi più elevati statisticamente significativi di urodilatina sono stati osservati anche quando i pazienti con RSW sono stati confrontati con gli altri due gruppi di pazienti considerati insieme (5,46 vs 0,32 ng/mL, test MW p<0,001). Al contrario, i livelli di proANP non erano statisticamente differenti tra i 3 sottogruppi (test KS complessivo p=0,266) o tra pazienti con RSW e pazienti con/senza iponatriemia (4,9 vs 9,7 nM, test MW p=0,122). Le prestazioni diagnostiche dei livelli medi di urodilatina per la diagnosi di RSW sono state valutate mediante la curva ROC. L'area sotto la curva (AUC) era 0,94 (IC 95% 0,86-1,00). Il miglior cut-off per i livelli medi di urodilatina, secondo l'indice di Youden, era di 2,87 ng/mL. A questo cut-off sensibilità, specificità, valore predittivo positivo e valore predittivo negativo erano, rispettivamente, 1,00, 0,88, 0,60 e 1,00. In conclusione, questo studio pilota ha mostrato risultati interessanti per quanto riguarda il dosaggio di urodilatina urinaria in pazienti con RSW, con implicazioni potenzialmente chiarificatrici e di utilità pratica sia per quanto riguarda la patogenesi di questa sindrome, sia per quanto riguarda i suoi criteri diagnostici e quindi sulla gestione clinica dei pazienti. Ci auguriamo che ulteriori studi futuri possano continuare a fare luce su questo interessante argomento.
Renal Salt Wasting Syndrome (RSW) is a clinical syndrome with laboratory characteristics completely overlapping with the syndrome of inappropriate ADH secretion (SIADH). The fundamental difference between the two syndromes lies in the extracellular volume (ECV), reduced in RSW and normal or slightly increased in SIADH. The difficulties in the differential diagnosis of this syndrome and in understanding the precise pathogenetic mechanism have contributed some authors to question the very existence of RSW. Considering the characteristics of RSW, natriuretic peptides were investigated to explain its onset such as ANP and BNP, with unsatisfactory results. However, no studies have yet investigated the possible role of urodilatin, a peptide belonging to the natriuretic peptide family, which seems to have a crucial role in regulating blood sodium and urinary sodium even more than ANP. We performed a retrospective observational study, the patients were divided into 3 groups: a group of patients without hyponatremia and two groups of patients with hyponatremia, one consisting of patients with RSW and the other consisting of patients with hyponatremia from other causes. patients with RSW display significantly higher mean urodilatin levels than both patients with (median 5.46 vs 0.57 ng/mL, p=0.006) or without hyponatremia (median 5.46 vs 0.27 ng/mL, p<0.001). Statistically significant higher mean levels of urodilatin were also observed when patients with RSW were compared with the other two groups of patients considered together (5.46 vs 0.32 ng/mL, MW test p<0.001). Conversely, proANP levels were not statistically different among the 3 subgroups (overall KS test p=0.266) or between patients with RSW and patients with/without hyponatremia (4.9 vs 9.7 nM, MW test p=0.122). Diagnostics performances of mean urodilatin levels for RSW diagnosis were evaluated by ROC curve. Area under the curve (AUC) was 0.94 (95%CI 0.86-1.00). Best cut-off for mean urodilatin levels, according to Youden’s index, was 2.87 ng/mL. At this cut-off sensitivity, specificity, positive predictive value and negative predictive value were, respectively, 1.00, 0.88, 0.60 and 1.00. In conclusion, this pilot study has shown interesting results regarding the dosage of urinary urodilatin in patients with RSW, with potentially clarifying implications and of practical utility both regarding the pathogenesis of this syndrome and regarding its diagnostic criteria and therefore on the clinical management of patients. We hope that further future studies can continue to shed light on this interesting topic.
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2

DE, VITO PAOLO. "Relazione tra pH intracellulare e produzione di specie reattive dell’ossigeno nella risposta immune innata: ruolo dello scambiatore sodio/idrogeno e del peptide natriuretico atriale." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2004. http://hdl.handle.net/2108/208231.

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Le cellule fagocitiche; monociti, macrofagi e neutrofili, sono i maggiori componenti della immunità innata. Tali cellule rispondono a stimoli infiammatori e/o immunitari attraverso meccanismi di difesa che si esplicano tramite la fagocitosi, la produzione di citochine e la generazione di specie reattive dell’ossigeno (ROS). I meccanismi di difesa operati dai fagociti sono selettivamente influenzati dal pH intracellulare (pHi) che è in genere regolato da differenti trasportatori di membrana tra cui lo scambiatore sodio/idrogeno (NHE). L’NHE opera l’influsso di ioni sodio ed il contemporaneo efflusso di ioni idrogeno in accordo con i rispettivi gradienti di concentrazione. Le funzioni di NHE non sono ristrette alla regolazione del pHi: lo scambiatore esercita anche un importante ruolo in diverse funzioni biologiche tra cui la proliferazione e il differenziamento cellulare, l’apoptosi e la riorganizzazione citoscheletrica. Inoltre, in diversi tumori, il microambiente extracellulare è più acido di quello che caratterizza i tessuti normali, e in queste condizioni l’NHE rappresenta l’unico sistema in grado di assicurare l’omeostasi del pHi. A questo riguardo, nel modello di carcinoma epatico umano (HepG2), i livelli di mRNA di NHE come l’attività dello scambiatore sono 10 e 3 volte superiori rispetto a quanto riportato per i normali epatociti. Variazioni del pHi in risposta a differenti agonisti possono rappresentare dei segnali precoci capaci di contribuire alla regolazione dell’attività delle fosfolipasi; una famiglia di enzimi in grado di generare dei lipidi bioattivi tra cui il diacilglicerolo (DAG) e l’acido fosfatidico (PA). Il DAG e il PA possono attivare l’enzima NADPH ossidasi, che rappresenta una importante sorgente di ROS nei fagociti. La NADPH ossidasi svolge un importante ruolo anche in altri sistemi cellulari tra cui le HepG2, dove la sua attivazione appare essere positivamente correlata all’inibizione della proliferazione cellulare. I monociti ed i macrogafi in risposta a degli stimoli infiammatori sono in grado di rilasciare il peptide natriuretico atriale (ANP), un piccolo ormone principalmente sintetizzato dai cardiomiociti atriali capace di promuovere la natriuresi, la diuresi e di contribuire alla regolazione della pressione sanguigna. L’ANP può anche regolare alcune funzioni immunitarie in quanto capace di contrastare l’espressione di alcuni mediatori infiammatori tra cui la ciclossigenasi-2 (COX2), l’ossido nitrico (NO) e il fattore di necrosi tumorale (TNF)-α.Sulla base dell’importante ruolo del pHi e della possibile relazione tra NHE e produzione di ROS, il presente studio è stato incentrato nel valutare l’effetto dell’ANP sul pHi, sull’attività di alcune fosfolipasi (Ce D) e sulla produzione di ROS nei monociti/macrofagi umani e nelle cellule HepG2. I risultati ottenuti hanno evidenziato un significativo decremento del pHi dovuto all’inibizione di NHE dopo stimolazione con ANP nei macrofagi e nelle cellule HepG2. Sia i monociti che i macrofagi si siano rivelati in grado di esprimere l’intero set dei recettori per i peptidi natriuretici (NPR-A,NPR-B e NPR-C), ma nessuna significativa variazione del pHi è stata evidenziata nei monociti stimolati con ANP. Tuttavia, il trattamento dei monociti con 5-(etil-N-isopropil)amiloride, uno specifico inibitore di NHE è stato in grado di riprodurre il modello di acidificazione osservato nei macrofagi dopo stimolazione con ANP. Nei macrofagi il decremento ANP-dipendente del pHi è apparso parallelo ad un incremento dell’attività della PLD e della PLC, mentre nelle cellule HepG2 l’acidificazione intracellulare è stata correlata unicamente dell’attivazione della PLD. Il decremento ANP-dipendente del pHi, è stato correlato alla produzione di messaggeri lipidici bioattivi quali il DAG e il PA che si sono dimostrati responsabili dell’attivazione della NADPH ossidasi sia nei macrofagi che nelle cellule HepG2. Infine, tutti gli effetti mediati dall’ANP sono stati riprodotti utilizzando un analogo troncato dell’ormone denominato cANF specifico per i recettori NPR-C.
Phagocytes, namely monocytes, macrophages, and neutrophils, are major components of innate immunity. They respond to inflammatory/immune insults by up-regulating their host defense functions, including phagocytosis, cytokine production, and generation of reactive oxygen species (ROS). The host defense functions of phagocytes are selectively influenced by intracellular pH (pHi) that is controlled by which several plasmamembrane acid-base transporters, including the Na+/H+ exchanger (NHE) which operate the exchange of extracellular Na+ with cytoplasmic H+ ions according to the concentration gradient. The functions of NHE are not only restricted to pHi homeostasis: the exchenger plays also an important role a variety of downstream events, including cell proliferation, cell differentiation, apoptosis, and cytoskeletal organization. Moreover, in several tumors, the extracellular microenviroment is more acidic with respect to normal tissues and, in these conditions, the NHE represents the only system able to regulate pHi homeostasis. In this contest, it was reported , in hepatocellular carcinoma (HepG2 cells), that NHE mRNA levels as well as the exchanger activity are respectively 10-and-3 fold higher than in normal hepatocytes, Changes in pHi in response to a variety of ligands may represent a signalling event for the regulation of phospholipase activities: a family of enzymes able to generate bioactive lipids such as diacyglycerol (DAG) and phosphatidic acid (PA). DAG as well as PA can activate the enzyme NADPHoxidase, an important source of ROS in phagocytes. The NADPHoxidase plays an important role also in other cell systems including HepG2, where its activation appears positively coupled to the inhibition cell proliferation. It is well known that monocytes and macrophages in response to inflammatory insults can release the atrial natriuretic peptide (ANP), an hormone mainly secreted by the heart atria able to induce natriuresis, vasodilation and contribute to the regulation of blood pressure. The ANP can also regulate several immune functions since its able to reduce production of proinflammatory mediators by inhibition of nitric oxide (NO), and cyclooxygenase-2 (COX2) as well as tumor necrosis factor (TNF)-α synthesis. On the basis of both the important role of pHi and the possible relationship between NHE and ROS generation, the present study was aimed to evaluate the effects of atrial natriuretic peptide (ANP) on intracellular pH (pHi), phospholipase (C and D) activities and (ROS) production in human monocytes, macrophages and HepG2 cells. A significant pHi decrease due to the NHE inhibition was observed in ANP-stimulated macrophages as well as in HepG2 cells. Conversely, even if both monocytes and macrophages were show to express all three natriuretic peptide receptors (NPR-A, NPR-B, and NPR-C), no significant effect on pHi was observed in monocytes stimulated with ANP. Nevertheless, the treatment of monocytes with 5-(N-ethyl-N-isopropyl)amiloride, a specific inhibitor of NHE was able to determine a decrease of pHi which was similar to the one observed in macrophages after ANP stimulation. In human macrophages the ANP-induced pHi decrease was paralleled by an increased activity of both phospholipase D (PLD) and phospholipase C (PLC), whereas in HepG2 cells the intracellular acidification was correlated only to an increased PLD activity. Our results suggest that second lipid messengers produced after ANP-induced pHi decrease, such DAG and PA, were able to promote the NADPH oxidase activation in human macrophages as well as in HepG2 cells. Finally, all ANP-effects were mediated by NPR-C receptors.
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3

Thompson, Justine Sarah. "Atrial natriuretic peptide and the pulmonary circulation." Thesis, University of Sheffield, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364381.

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4

Zhang, Jin. "Inhibition of pulsatile luteinizing hormone release by atrial natriuretic peptide and brain natriuretic peptide in the ovariectomized rat." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29412.

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Atrial natriuretic peptide (ANP) of atrial myocyte origin, has been shown to play a role in the diuresis, natriuresis, and antagonism of angiotensin and vasopressin. However, it is now apparent that in addition to the production of the peptide in the heart and in its role in fluid and electrolyte homeostasis, it is also produced in the central nervous system participating in the regulation of pituitary hormone secretion. Administration of ANP through both central and peripheral routes has been shown to inhibit secretion of luteinizing hormone (LH) in the gonadectomized rat model. A better understanding of the modulatory role of ANP on LH secretion and its possible mechanisms will add to our knowledge of the effects of neuropeptides on reproductive function. Brain natriuretic peptide (BNP) is a bioactive peptide of 26 amino acid residues recently identified in porcine brain. The peptide exerts potent diuretic-natriuretic and vasorelaxant effects, in a manner similar to that of ANP. BNP has a remarkable high sequence homology to ANP, especially in the 17 amino acid ring formed by an intramolecular disulfide linkage which is required for biological activity. The presence of BNP with ANP in the mammalian brain and remarkable resemblance in their molecular structures and physiological functions implies that BNP may also exert an inhibitory effect on LH secretion like ANP. This research focused on the effects of centrally administered ANP and BNP on pulsatile LH secretion and their possible mechanisms of action in ovariectomized rats. After third ventricle infusion of ANP or BNP, inhibition of mean plasma LH level, LH pulse amplitude and pulse frequency was observed. In searching for the possible mechanisms of inhibitory effect of ANP or BNP on pulsatile LH secretion, the effect of inhibiting the endogenous opiate system with naloxone on the action of centrally administered ANP or BNP was tested. Application of naloxone reversed the inhibitory effect of ANP and BNP on mean plasma LH level and LH pulse amplitude, but in terms of pulse frequency, naloxone treatment failed to reverse the inhibitory effect of ANP or BNP. In separate experiments, pretreatment with pimozide, a dopaminergic receptor blocker, prevented the inhibitory action of ANP and BNP on LH secretion. After infusion of ANP or BNP, there were no significant decrease in mean plasma LH level, pulse amplitude and pulse frequency in the pimozide-pretreated rats. In summary, the present study shows that both ANP and BNP inhibit pulsatile LH secretion, suggesting that the inhibitory effects on LH secretion once thought to be mediated by ANP alone may be regulated through a dual mechanism involving both ANP and BNP. Furthermore, the inhibitory mechanisms may involve the interactions of ANP and BNP with central opiate system and dopaminergic system on LH secretion.
Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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5

Kao, Jonathan. "Atrial natriuretic peptide in aging rats : evidence for altered processing, secretion and receptor binding." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28993.

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The recently discovered atrial natriuretic peptide (ANP) has potent diuretic, natriuretic and hypotensive effects, and is believed to be involved in the maintenance of sodium homeostasis in both normal and pathological conditions. The mammalian aging process is associated with a host of abnormalities that include, among others, a compromised ability to regulate sodium homeostasis. There are reports that demonstrate a positive correlation between plasma ANP levels and age in man; accordingly, the aim of this study was to examine whether age-related sodium imbalance is associated with disturbances in the homeostasis of ANP. Specifically, the intracellular storage, processing and secretion of ANP from the atrium was studied and associated with circulating ANP concentrations and ANP receptor binding kinetics. Studies were conducted with four groups of male Wistar rats designated as 1-, 3-, 10-, and 20-month-old. 24-hour renal clearances were conducted to assess age-related changes in renal functions. GFR and UNaV increased steadily from 1 to 10 months of age and decreased in the 20-month-old, while fractional excretion of water (FEH₂O) and sodium (FENa) declined initially (from 1 to 10 months) and then rose in the 20-month-old group. Circulating ANP levels in the rats was significantly correlated with the increase in age (N = 147, r = 0.59, p < 0.0005). Atria of the animals were isolated and superfused with a modified Langendorff apparatus. The spontaneous release of ANP increased from 1 to 3 months, and steadily decreased after 3 months. The results indicate that ANP secretion increases with maturation and thereafter declines with advancing age. ANP concentrations in the right and left atria were also quantified. The results revealed that atrial ANP content increased from 1 to 3 months and decreased progressively with age. There was a positive correlation between the rate of ANP release and atrial ANP content (N= 42, r=0.50, p<0.01), suggesting that the release of ANP from the right atrium was associated with the atrial content. The concurrence of a reduction in ANP secretion but with elevation in plasma ANP concentration in the aged (20-month-old) rats, suggests that there may be an impairment in renal clearance of ANP. It was established that the main molecular species present in the atrium was γ-ANP and that this was unaffected by age as assessed by reverse-phase high performance liquid chromatography (RP-HPLC) coupled with radioimmunoassay. The molecular forms of ANP secreted by the atrium consisted of predominantly α-ANP, with a smaller amounts of γ-ANP. γ-ANP constituted only 1% of the total secreted ANP in the 1-, 3-, or 10-month-old rats, but up to 8% was detected in 20-month-old rats. Although both α-ANP and γ-ANP were present in the circulation, the ratio of γ-ANP/α-ANP increased significantly with age. The concentration of γ-ANP in the plasma of the 20-month-old rats was two- to three-fold higher than in the two younger groups (1- and 3-month-old). These data imply that the post-transcriptional processing of prohormone γ-ANP to active α-ANP is altered with age. Radio-ligand binding experiments were carried out using glomerular ANP receptors to determine whether the age-related alterations in plasma ANP levels has an effect on the binding of ANP to its target tissues. Both the receptor density (Bmax) and the equilibrium dissociation constant (kd increased from 1 to 3 months but decreased from 3 to 20 months. Collectively, these results suggest that: 1) Aging affects atrial ANP content and consequently influences the release of ANP from the isolated atria. 2) The processing of prohormone γ-ANP to active α-ANP is modified with age. 3) Plasma levels of ANP increase with age, which may result in down-regulation of ANP receptor density and increased efficacy in receptor binding affinity. These may represent the compensatory responses.
Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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6

Hetmanski, David John. "A study of atrial natriuretic peptide in pregnancy." Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335300.

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7

Peters, Christian G. "SNARE-Mediated Exocytosis of Atrial Natriuretic Peptide from Atrial Cardiac Myocytes." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1179405759.

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8

Willeit, Peter. "Natriuretic peptides and cardiovascular disease." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648533.

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9

Taskinen, P. (Panu). "Mapping the cellular mechanisms regulating atrial natriuretic peptide secretion." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:9514252721.

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Abstract Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are cardiac hormones, which are involved in the regulation of blood pressure and fluid homeostasis. The major determinant for ANP and BNP release are atrial and ventricular wall stretch, but also some vasoactive factors such as endothelin-1 (ET-1) can enhance cardiac hormone secretion. The mechanical stretch rapidly activates multiple signal transduction pathways in cardiac cells, but the cellular mechanisms mediating stretch-induced ANP secretion are still unknown. The aim of the present study was to examine the cellular mechanisms of autocrine/paracrine factors and stretch-induced ANP secretion. Genistein, a potent protein tyrosine kinase (PTK) inhibitor, rapidly increased cardiac contractile force and ANP secretion in perfused rat heart. This effect of genistein may be unrelated to the inhibition of PTKs since this stimulation was blocked by a L-type calcium channel antagonist and Ca2+/calmodulin-dependent protein kinase II inhibitor. Pregnancy hormone relaxin increased heart rate and ANP secretion in perfused spontaneously beating heart, suggesting that relaxin may have a role in modulating cardiac function. Cellular mechanisms of atrial wall stretch-induced ANP secretion were also studied. This enhanced secretion was blocked by sarcoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin and PTK inhibitor lavendustin A, indicating that thapsigargin sensitive Ca2+ pools and activation of PTK orPTK cascade have an important role in the regulation of stretch-secretion coupling. In addition, protein phosphatase inhibitor okadaic acid accelerated stretch-induced ANP secretion, suggesting that precise balance of protein kinase and phosphatase activity plays a role in mechanical stretch-induced ANP secretion. Finally interactions of endothelial factors regulating ANP exocytosis were studied. The potent nitric oxide synthase inhibitor L-NAME increased basal and atrial wall stretch-induced ANP secretion in the presence of ET-1, suggesting that nitric oxide may tonically inhibit ANP secretion.
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Vaillancourt, Patrice A. "Modulation of atrial natriuretic peptide receptors in rat pregnancy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0006/MQ44307.pdf.

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11

Black, Leslie Seale. "Atrial natriuretic peptide and streptozotocin-induced diabetes in rats." Thesis, This resource online, 1991. http://scholar.lib.vt.edu/theses/available/etd-08182009-040300/.

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Vaillancourt, Patrice A. "Modulation of atrial natriuretic peptide receptors in rat pregnancy." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=20886.

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The mechanisms underlying the net fluid/electrolyte gain during pregnancy are not fully understood. Utilizing virgin, pregnant (7, 16 and 21 days gestation), estradiol-17beta- or progesterone-treated female rats, we have examined the role of atrial natriuretic peptide (ANP) and of its receptors in the adaptation of body fluid homeostasis during pregnancy. Pregnancy and progesterone attenuate the ANP-mediated inhibition on aldosterone production in adrenal zona, glomerulosa (ZG) cells. The ribonuclease protection assay and Western analysis revealed that ZG natriuretic peptide guanylyl cyclase-linked (GC) receptors are mainly GC-A and that they are downregulated by pregnancy. In addition, pregnancy downregulates GC-A and GC-B receptors in the uterus; however, it does not modulate GC-linked receptors in the lung. It is concluded that the downregulation of ZG GC-A receptors could lead to a decrease in the aldosterone-suppressant effects of ANP and that the decrease in uterine GC-A and GC-B receptors could lead to a decrease in the tocolytic effects of ANP during pregnancy.
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Vries, Petrus Johannus Fransciscus de. "Atrial natriuretic peptides their role in cardiovascular homeostasis /." Maastricht : Maastricht : Datawyse ; University Library, Maastricht University [Host], 1990. http://arno.unimaas.nl/show.cgi?fid=6192.

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14

McCartney, Shirley. "Atrial natriuretic peptide receptor subtype determination and biological actions of atrial natriuetic peptided in bovine cardiac muscle and hypertensive rat liver." Thesis, University of St Andrews, 1992. http://hdl.handle.net/10023/14455.

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Atrial natriuretic peptide (ANP) has previously been shown to bind to specific ANP receptors and increase intracellular cGMP levels in purified rat cardiac sarcolemmal membranes. Experiments described in this thesis were performed to investigate the binding characteristics of ANP in bovine ventricular sarcolemmal membranes and in plasma membranes isolated from the liver of hypertension-resistant and hypertension-sensitive Dahl rats fed on two dietary salt regimes one of 0.8% NaCl and the other 8% NaCl. Additional experiments utilising ANP analogues in radio-receptor assays and radio-receptor crosslinking assays were performed to determine the precise nature of the ANP receptor population present in these membrane preparations. In bovine ventricular cardiac sarcolemmal membranes, ANP bound specifically to one class of ANP receptor with a Kd of approximately 44 pM and a Bmax of approximately 49 fmol/mg protein. ANP produced a 1.8-fold stimulation of manganese-dependent guanylate cyclase activity with an EC50 value of approximately 1 nM. Receptor binding using the des-ANP analogue indicated the predominant presence of the ANP-B receptor subtype. Radioreceptor crosslinking experiments did not entirely agree with these experiments. Radio-receptor crosslinking indicated the presence of two ANP receptors one of 60 kDa and one of 120 kDa, equivalent to the molecular weights of ANP receptors found in other tissues. Collectively these experiments indicate that bovine ventricular sarcolemmal membranes possess ANP receptors, at least a proportion of which are coupled to guanylate cyclase (ANP-B receptors). In plasma membranes from the liver of Dahl-Resistant (Dahl-R) and Dahl-Sensitive (Dahl-S) rats, ANP bound specifically to one class of ANP receptor with Kd values ranging from 245 to 288 pM and Bmax values ranging from 104 to 217 fmol/mg protein. ANP produced a 3.8 to 6.15-fold stimulation of manganese-dependent guanylate cyclase activity with an EC50 values ranging from 2.3 to 7.4 nM, dependent on the strain of Dahl rat and the dietary salt regime used. In liver membranes isolated from rats sensitive to salt-induced hypertension results indicated increases in Bmax with no change in Kd for ANP binding to receptors and higher basal and ANP-stimulated guanylate cyclase levels. Receptor binding using the des-ANP analogue indicated the presence of 13-33% ANP-C receptors with a majority of ANP-B receptors in plasma membranes isolated from the liver of Dahl-R and Dahl-S rats. However, radio-receptor crosslinking experiments were unable to support these results. Collectively these experiments indicate that in plasma membranes isolated from the liver of Dahl-R and Dahl-S rats possess ANP receptors, at least a majority of which are coupled to guanylate cyclase (ANP-B receptors) and that sensitivity to hypertension induced by a high salt dietary regime increases the density of ANP receptors coupled to guanylate cyclase.
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15

Cheung, Bernard Man Yung. "Comparison of the roles of atrial natriuretic factor and brain natriuretic peptide in man." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387503.

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16

Irons, D. W. "Atrial natriuretic peptide in normal & pre-eclamptic human pregnancy." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321262.

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Suda, Susanne. "Atrial natriuretic peptide in mild to moderate chronic renal failure /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Thomas, Colleen J(Colleen Joy) 1965. "Influence of natriuretic peptides on cardiac reflexes." Monash University, Dept. of Physiology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8347.

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Koch, Elke. "Influence of Atrial Natriuretic Peptide on inflammatory pathways in the lung." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-53485.

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Zhao, Jing. "A-type receptor of atrial natriuretic peptide in spontaneously hypertensive rat." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627461.

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21

Park, Kwijun. "Therapeutic potential of atrial natriuretic peptide administration on peripheral arterial diseases." Kyoto University, 2008. http://hdl.handle.net/2433/135849.

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Gnädinger, Markus Peter. "Plasma kinetics of synthetic alpha-human atrial natriuretic peptide in man /." [S.l : s.n.], 1985. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Rugg, Elizabeth Louise. "Biochemical actions and degradations of atrial natriuretic peptide in rat tissues." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/14453.

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Atrial natriuretic peptide (ANP) has previously been shown to increase intracellular cGMP levels in isolated rat ventricular myocytes. Using purified rat cardiac sarcolemmal membranes, a series of experiments was performed to investigate the mechanisms by which this occurs. A second series of experiments was carried out to investigate the nature of ANP degradation by preparations isolated from rat heart, lung and kidney. In rat cardiac sarcolemmal membranes, ANP produced a 1.8-fold stimulation of manganese-dependent guanylate cyclase activity, with a Km of around 1nM. This activity was attenuated by the presence of 1 nM ATP in the incubation. In the presence of magnesium, guanylate cyclase activity was reduced 20- to 40-fold, but was augmented by ATP. Similar results were obtained in the presence of ANP-PNP, a non-hydrolysable analogue of ATP. [125I]-ANP binding studies indicated the presence of two receptor/affinity states, with KD'S of less than 10 pM, and around 1 nM for the high and low affinity sites respectively. More than 90% of these receptors were of the low affinity form. Similar results were obtained with bovine adrenal cortex membranes, but with MDCK cell membranes, only high affinity binding sites could be detected. These experiments indicate that rat cardiac sarcolemmal membranes possess ANP receptors, at least a proportion of which are coupled to guanylate cyclase. Incubation of [125I]-ANP with isolated rat ventricular myocytes, or with a cytosolic fraction prepared from these cells, resulted in its rapid degradation. The proteolytic activity appeared to be due to the action of a soluble metallopeptidase. Incubation of [125I]-ANP with a cytosolic fraction prepared from rat kidney and lung indicated that similar degradative activity could be isolated from these tissues.
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Janssen, Wilbert Martien Theodoor. "Atrial natriuretic factor integrated effects on blood pressure, natriuresis, and renal medullary blood flow in man /." [S.l. : [Groningen] : s.n.] ; [University Library Groningen] [Host], 1994. http://irs.ub.rug.nl/ppn/123950805.

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25

楊鐸輝 and Tok-fai Vincent Yeung. "Aspects of the biological interactions between natriuretic peptides and cultured glial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31981665.

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Yeung, Tok-fai Vincent. "Aspects of the biological interactions between natriuretic peptides and cultured glial cells." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18650302.

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Man, Bik-ling. "Plasma brain natriuretic peptide and systemic ventricular function after the Fontan procedure /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34865822.

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Béland, Mireille. "Plasma atrial natriuretic peptide during brief upright and supine exercise in man." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61984.

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Hasler, Loretta. "Blood levels and renal effects of atrial natriuretic peptide in normal man /." [S.l : s.n.], 1985. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Ye, Xiadi. "Genetic analysis of natriuretic peptides and blood pressure in the spontaneously hypertensive rat /." [St. Lucia, Qld.], 2000. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16801.pdf.

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31

Gerwig, Tobias. "Prevention of Ischemia-Reperfusion Injury in the Rat Liver by Atrial Natriuretic Peptide." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-888.

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Tattersall, James Erskine. "Atrial natriuretic peptide : its measurement in plasma and role in blood volume homeostasis." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338515.

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Rosenzweig, Ivana. "An investigation into the role of atrial natriuretic peptide in wound and healing." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621845.

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Hulks, Geoffrey. "The effect of atrial natriuretic peptide on airway tone and reactivity in man." Thesis, University of Dundee, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294773.

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Tsuneyoshi, Hiroshi. "Atrial natriuretic peptide (ANP) helps prevent late remodeling after left ventricular aneurysm repair." Kyoto University, 2005. http://hdl.handle.net/2433/144751.

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36

Man, Bik-ling, and 文碧玲. "Plasma brain natriuretic peptide and systemic ventricular function after the Fontan procedure." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010365.

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MacLean, Heidi Norma. "Plasma N-terminal Proatrial Natriuretic Peptide Concentration in Cats with Hypertrophic Cardiomyopathy." Thesis, Virginia Tech, 2004. http://hdl.handle.net/10919/31538.

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Objective: We sought to determine N-terminal proatrial natriuretic peptide concentrations [Nt-proANP] in plasma from cats with hypertrophic cardiomyopathy (HCM). Secondarily, we wished to evaluate the relationship between [Nt-proANP] and echocardiographic variables. Methods: Venous blood samples were obtained from seventeen cats with HCM and from nineteen healthy cats. Plasma [Nt-proANP] was determined using an ELISA assay. The relationship between plasma [Nt-proANP] and M-mode, 2-dimensional and Doppler echocardiographic variables was evaluated. Cats that were hyperthyroid or had evidence of renal disease were excluded from the study. Results: The mean plasma [Nt-proANP] was higher in cats with HCM (3.81 +/- 1.23 pmol/l) than in control cats (3.08 +/- 1.41 pmol/l); however, this difference was not statistically significant (p=0.17). There was a significant correlation between plasma [Nt-proANP] and left ventricular posterior wall thickness (r = 0.42; p=0.01). Additionally, plasma [Nt-proANP] was correlated with left atrial size (r = 0.35; p=0.03). A linear regression model was developed to further explore these relationships. LAs2D and LVPWd had an interactive effect on plasma [Nt-proANP] (R2 = 0.2737; p= 0.02). There was no correlation between any other echocardiographic variable and plasma [Nt-proANP]. There was no correlation between plasma [Nt-proANP] and heart rate (HR), body-weight, or age. Conclusions: Cats with HCM do not have significantly higher plasma [Nt-proANP] than normal cats. There was a significant linear relationship between [Nt-proANP] and LAs2D, LVPWd and the model that described their interaction.
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Wu, Shengqian. "Study of atrial natriuretic peptide and endothelin in streptozotocin-diabetic rats and in the aging rats /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19982069.

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Model, Angela Nikola. "Die Regulation der ANP-Freisetzung bei Herzinsuffizienz." Doctoral thesis, [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976580187.

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Weber, Nina Claudia. "Influence of the Atrial Natriuretic Peptide on TNF- αα α -activated human endothelial cells." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-808.

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Mbanya, J.-C. N. "Atrial natriuretic peptide, sodium and erythrocyte membrane transport in hypertension associated with diabetes mellitus." Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233334.

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Macaulay, Hunter Esther Frances. "The measurement of Pro Atrial Natriuretic Peptide and derived peptides, in health and heart disease, using several 'two-site' immunoradiometric assays and radioimmunoassays." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357706.

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Keller, Melanie. "Cytoprotective and Anti-Inflammatory Properties of the Atrial Natriuretic Peptide during Ischemia/Reperfusion and Endotoxemia." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-47771.

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Aoyama, Akihiro. "Post-ischemic Infusion of Atrial Natriuretic Peptide Attenuates Warm Ischemia-Reperfusion Injury in Rat Lung." Kyoto University, 2011. http://hdl.handle.net/2433/142544.

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45

JÃnior, Raimundo Campos Palheta. "CaracterizaÃÃo das vias neuro-humorais no retarde do esvaziamento gÃstrico de lÃquidos advindo da distensÃo mecÃnica atrial direita em ratos acordados." Universidade Federal do CearÃ, 2010. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=4180.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
A distensÃo mecÃnica do Ãtrio direito (DA) aumenta a motilidade gÃstrica em ratos anestesiados (Palheta et al., 2010). Resolvemos avaliar o efeito da DA sobre o esvaziamento gÃstrico (EG) de lÃquido em ratos acordados e as eventuais vias neuro-humorais relacionadas ao fenÃmeno. Utilizamos ratos albinos machos (n=361, 250-280g) que receberam um balÃo de silicone posicionado no Ãtrio direito. Decorridos 24h, monitoramos a pressÃo venosa central (PVC), freqÃÃncia cardÃaca (FC) e a pressÃo arterial mÃdia (PAM) e apÃs os 20-min iniciais os animais foram aleatoriamente prÃ-tratados com: Salina (S, 0,1 ml/100g, i.v.), Atropina (A, 0,5 mg/kg, i.v.), Guanetidina (GT, 10 mg/kg, i.p.), HexametÃnio (H, 10mg/kg, i.v.), L-NAME (3mg/kg, i.v.), L-Arg (100mg/kg, i.v.) + L-NAME (3 mg/kg, i.v.), Azul de metileno (MB, 3 mg/kg, i.v.), Glibenclamida (GB, 1 mg/kg, i.p.) ou Glibenclamida + DiazÃxido (3mg/kg, i.v.) [GB + D], Dexametasona (DEX, 1mg/kg, i.p.), Anantin (ANT, 5 g, i.v.) ou Atosibana (AT, 40  g/kg/h, i.v.). AlÃm disto, em grupos separados realizamos 72h antes da DA Ã vagotomia (V), ou esplancnotomia+ gangliectomia celÃaca (SC) ou denervaÃÃo cardÃaca aferente com capsaicina (ACD). Em outro conjunto de animais realizamos aurilectomia direita uma semana antes da DA (AX). Em seguida ao tratamento farmacolÃgico realizamos protocolo de falsa DA (controle) ou DA com 50L do balÃo intra-atrial durante 5min. Decorridos 20 min. da DA, os ratos foram alimentados por via oral com soluÃÃo teste e, apÃs 10-min sacrificados para estudo do EG. AlÃm disto, determinamos os nÃveis plasmÃticos de ocitocina (OT), PeptÃdeo NatriurÃtico Atrial (ANP) e corticosterona (CORT). Para verificaÃÃo da atividade neuronal avaliamos a expressÃo da proteÃna Fos e OT nas regiÃes hipotalÃmicas do nÃcleo paraventricular (PVN) ou supra-Ãptico (SON). Comparado ao controle, a DA diminuiu o EG (p <0,05). AlÃm disso, a DA aumentou a PVC e a FC. A DA diminuiu o EG (p<0,05) nos grupos S, A, GT, L-arginina + L-NAME, MB e GB+D. JÃ o prÃ-tratamento com H, L-NAME, GB, DEX, ANT ou AT, bem como a SV, SC, ACD ou AX preveniu o efeito do DA sobre o EG. AlÃm disso, a DA aumentou os nÃveis plasmÃticos de OT e CORT, mas nÃo alterou o de ANP. Apesar da DA aumentar o nÃmero de neurÃnios imunorreativos para c-fos nas regiÃes parvocellular medial e posterior do PVN, nÃo observamos tal achado nas regiÃes magnocellular do PVN ou do SON, tambÃm nÃo houve diferenÃa significativa para o nÃmero de neurÃnios imunorreativos para Fos-OT apÃs DA. Portanto a diminuiÃÃo do EG de lÃquidos apÃs a DA em ratos acordados depende de uma via aferente cardÃaca mediada por receptores de baixa pressÃo, sendo que tanto neurÃnios simpÃticos como parassimpÃticos participam da cascata mediada pela OT, ANP e NO atravÃs de canais para K+-ATP dependentes.
Right atrium mechanical stretch (AS) increases gastric motility in anesthetized rats. We aimed to study the effect of AS on gastric emptying (GE) in awake rats and the related neuro-humoral pathways ivolved. Male albino rats (N=361, 250-280g) had a silicone balloon inserted in the right atrium. After 24-h, the central venous pressure (CVP), heart rate (HR) and the mean arterial pressure (MAP) were monitored and after the initial 20-min, animals were randomly pre-treated with: saline (S, 0.1 ml/100g, i.v.), Atropine (A, 0.5mg/kg, i.v.), Guanethidine (GT, 10mg/kg, i.p.), hexamethonium (H, 10mg/kg, i.v.), L-NAME (3mg/kg, i.v.), L-Arginine (100mg/kg, i.v.)+L-NAME (3mg/kg, i.v.), Methylene Blue (MB, 3mg/kg, i.v.), Glibenclamide (GB, 1mg/kg, i.p) or Glibenclamide+Diazoxide (3mg/kg, i.v.) [GB+D], Dexamethazone (DEX, 1mg/kg, i.p.), Anantin (ANT, 5g, i.v.) or Atosiban (AT, 40g/kg/h, i.v.). Besides, in a separate group, we realized vagotomy (V), or splanchnotomy + celiac gangliectomy (SC) or afferent cardiac denervation with capsaicin (ACD) 72h before AS. In another set of animals, we realized right appendectomy (AX) one week before AS. Next, AS with saline zero (sham) or 50L was performed during 5min. In this group, rats were gavage fed with a test meal 20-min after AS and euthanized 10-min afterwards to study GE. Moreover we determined plasmatic levels of Ocytocin (OT), Atrial Natriuretic Peptide (ANP) and Corticosterone (CORT), and determined the neuronal activity in the paraventricular (PVN) or supraoptic (SON) hypothalamic regions by measuring expressed double-labeled c-fos-OT. Comparing to Sham, AS decreased GE (p<0.05). Besides, AS increased CVP and HR. AS decreased GE (p <0.05) in S, A, GT, L-Arginine+L-NAME, MB and GB+D groups. However pre-treatment with, H, L-NAME, GB, DEX, ANT or AT, as well as SV, SC, ACD or AX prevented the effect of AS on GE. AS increased OT and CORT plasmatic levels, but did not alter ANP. In spite of AS increasing the number of c-fos expressing neurons in the parvocellular region, we did not observe this finding in the magnocellular regions of PVN or SON. Besides, AS did not alter the number of fos-OT double-labeled neurons. Therefore the decrease of GE of fluids after AS in awake rats depends on an afferent pathway mediated by cardiac low pressure receptors, and both sympathetic and parasympathetic neurons participate in the cascade mediated by OT, ANP and NO through K +-ATP dependent channels.
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46

Doust, Jenny. "Managing uncertainty in diagnostic decision making : B-type natriuretic peptide for the diagnosis and management of heart failure /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19791.pdf.

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47

吳勝前 and Shengqian Wu. "Study of atrial natriuretic peptide and endothelin in streptozotocin-diabetic rats and in the aging rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237885.

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48

Uehlinger, Claudius Jeckelmann-Wiesendanger Katrin. "Effects of aldrenalectomy, renal denervation and atrial natriuretic peptide in ischemic renal failure in the rat /." Bern, 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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49

Hijazi, Ziad. "New Risk Markers in Atrial Fibrillation." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198833.

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Atrial fibrillation (AF) confers an independent increased risk of stroke and death. The stroke risk is very heterogeneous and current risk stratification models based on clinical variables, such as the CHADS2 and CHA2DS2VASc score, only offer a modest discriminating value. The aims of this thesis were to study cardiac biomarkers, cardiac troponin and natriuretic peptides e.g. N-terminal prohormone-B-type natriuretic peptide (NT-proBNP), and describe levels in AF patients, investigate the association with stroke or systemic embolism, cardiovascular event, major bleeding and mortality, and to assess how levels of cardiac biomarkers change over time. Cardiac troponin was analyzed with contemporary assays and high sensitivity assays. The study populations consisted of patients with atrial fibrillation and one risk factor for stroke included in the RE-LY (n=6189) and the ARISTOTLE (n=14892) biomarker substudies. Median follow-up time was 2.2 years and 1.9 years, respectively. In a subset of participants (n=2514) data from repeated measurements was available at three months. Cardiac troponin was detectable in 57.0% with the contemporary assay and 99.4% with the high sensitivity assay. NT-proBNP was elevated in approximately three quarters of the participants. In Cox models adjusted for established risk factors the cardiac biomarkers levels was independently associated with stroke or systemic embolism, cardiovascular events, and mortality. Only cardiac troponin was associated with major bleeding. In ROC analyses the prediction of stroke or systemic embolism, cardiovascular events, and mortality increased significantly by addition of cardiac troponin or NT-proBNP to the models. Persistent detectable cardiac troponin (contemporary assay) and elevated NT-proBNP levels were found in a large number of participants. Persistent detectable or elevated levels conferred significantly higher risk for stroke or systemic embolism, cardiovascular events, and mortality. By using both cardiac biomarkers simultaneously the risk stratification improved even further for all outcomes. In conclusion the analyses for the first time display that elevation of troponin I and NT-proBNP are common in patients with AF and independently related to increased risks of stroke, cardiovascular events and mortality. Persistent elevation of troponin and NT-proBNP indicate a worse prognosis than transient elevations or no elevations of either marker. The cardiac biomarkers added substantial improvements to existing risk stratification models.
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50

Singer, Donald Robert James. "Studies of the importance of atrial natriuretic peptides in physiology, pathophysiology and treatment in man." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262349.

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In this thesis an attempt has been made to try to dissect out the relative importance of atrial natriuretic peptides (ANP) and the renin-angiotensin-aldosterone system in the control of sodium balance in normal man. At the same time the thesis examines the relevance of ANP in the pathophysiology of essential hypertension and cardiac transplantation and the potential therapeutic value of manipulating the ANP system. The studies described in this thesis were important in suggesting a dominant role of suppression of the renin-angiotensin-aldosterone system in permitting excretion of short term increases in intravenous or oral sodium intake. The permissive effects of suppression of angiotensin II or aldosterone for the excretion of an intravenous sodium load showed clear time differences, with suppression of angiotensin II important immediately but the response to suppression of aldosterone delayed. In contrast, there appears to be only a transient role for changes in circulating levels of ANP in the response to an intravenous sodium load and little evidence that changes in ANP release are important in responding to acute increases in dietary sodium intake in normal subjects. However, the sensing mechanism for ANP release is clearly activated by sustained changes in dietary sodium intake. Studies of prolonged dietary sodium alteration in normal subjects clear evidence for a role of ANP in the medium term regulation of sodium balance and further dietary studies suggested an important role for the ANP system in pathophysiology in essential hypertension and in cardiac transplant recipients.
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