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Thomas Maack - One of the best experts on this subject based on the ideXlab platform.
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role of atrial natriuretic factor in volume control
Kidney International, 1996Co-Authors: Thomas MaackAbstract:Atrial natriuretic factor (ANF) is a 28 amino acid polypeptide hormone secreted mainly by the heart atria in response to atrial stretch. ANF acts on the kidney to increase sodium excretion and GFR, to antagonize renal vasoconstriction, and to inhibit renin secretion. In the cardiovascular system, ANF antagonizes vasoconstriction, and shifts fluid from the intravascular to the interstitial compartment. In the adrenal gland, ANF is a powerful inhibitor of aldosterone synthesis. ANF participates importantly in the natriuretic response to acute and chronic volume overload. ANF's property of shifting fluid from the vascular to the interstitial compartment acts as a buffering device, guarding against excessive plasma volume expansion in face of an increased total extracellular fluid volume. ANF is also a physiological modulator of GFR, and mediates nephron hyperfiltration and natriuresis when salt excretion is threatened by a reduction in the number of nephrons. Guanylyl cyclase (GCA) receptors mediate the effects of ANF by generating cGMP. Clearance receptors remove ANF from the circulation by receptor-mediated endocytosis, and serve as a hormone buffer system to impede large inappropriate fluctuations in plasma levels of ANF. The specific structure-function-dynamics relationships of these receptors serve to modulate the role of ANF in pressure-volume homeostasis.
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receptors of atrial natriuretic factor
Annual Review of Physiology, 1992Co-Authors: Thomas MaackAbstract:Atrial natriuretic factor (ANF) is a polypeptide hormone that is secreted mainly by the heart atria in response to increases in atrial pressure or atrial stretch. ANF has multiple actions in the kidney that lead to increases in glomerular filtration rate and excretion of fluid and electrolytes, modulation of renal vascular resistance, decreases in inner medullary hypertonicity and sodium reabsorption by tubular epithelial cells, and stimulation of sodium secretion in inner medullary collecting duct cells. ANF also modulates systemic vascular resistance, inhibits the renin-angiotensin-aldosterone sys tem, and decreases arterial blood pressure, cardiac output and plasma volume (for a general review on the functional properties of ANF see Reference 11). Not surprisingly, after the initial reports in 1984 that showed the presence of high affinity specific binding sites of ANF in kidney cortex, aorta, and adrenal glomerulosa (30, 71), and the finding that ANF increases cGMP by activation of a membrane bound (particulate) guanylate cyclase (70, 107, 110), workers performed intensive and extensive studies on the distribution and the biochemical and functional properties of ANF receptors. These studies brought many novel concepts on receptor structure and function, whose full implication is still not understood. In this chapter, the main findings of these studies on ANF receptors and second messengers are considered in a brief and non-inclusive manner.
Christopher C Glembotski - One of the best experts on this subject based on the ideXlab platform.
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involvement of multiple cis elements in basal and α adrenergic agonist inducible atrial natriuretic factor transcription roles for serum response elements and an sp 1 like element
Circulation Research, 1995Co-Authors: Amy B Sprenkle, Susan F Murray, Christopher C GlembotskiAbstract:Abstract In the present study, cis elements in the 5′-flanking sequence (FS) of the rat atrial natriuretic factor (ANF) gene involved in regulating basal and α1-adrenergic–inducible transcription were investigated. Truncation analyses using ANF-luciferase reporter constructs transfected into primary neonatal rat cardiac myocytes showed that an A/T-rich serum response element (SRE) at −114 bp of the ANF 5′-FS, which bound serum response factor (SRF), was required for basal and inducible transcription. In constructs composed of 134 bp of rat ANF 5′-FS driving luciferase (ANF-134Luc), mutations in the SRE at −114 bp disrupted SRF binding and ANF promoter activity. However, the same mutations in ANF-638Luc had little effect, suggesting a collaborating role for more distal sequences, such as the other SRE in ANF-638 at −406 bp. In ANF-638Luc, mutations in the SRE at −406 bp that disrupted SRF binding to that site decreased ANF reporter activity by only 25%; however, mutating both of the SREs completely blocked α1-adrenergic–inducible activity. Mutation analyses showed that an ••• (SP-1)–like site at −69 bp, shown previously to confer inducibility in reporters with 134 bp of ANF 5′-FS, was not required in ANF-638Luc. However, double mutants in the SP-1–like region and either SRE completely blocked α1-adrenergic–inducible ANF promoter activity. These findings emphasize that no single element is responsible for α1-adrenergic agonist–regulated ANF transcription but that the SREs at −114 and −406 bp and the SP-1–like sequence at −69 bp mediate the effect in collaboration.
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involvement of cytoplasmic calcium and protein kinases in the regulation of atrial natriuretic factor secretion by contraction rate and endothelin
Journal of Biological Chemistry, 1994Co-Authors: Patrick M Mcdonough, Salvatore L Stella, Christopher C GlembotskiAbstract:To characterize the effects of the cellular events associated with contraction on atrial natriuretic factor (ANF) secretion, primary neonatal rat atrial myocytes were electrically paced to contract while being monitored for ANF release, cytoplasmic calcium, phosphoinositide hydrolysis, and protein kinase C activation. Similar measurements were also carried out in the presence of endothelin-1 (ET) for comparison of contraction-related and hormone-stimulated ANF secretion. Pacing (6-8 Hz) immediately increased ANF secretion by 3-5-fold and the time-averaged cytoplasmic calcium concentration (as monitored with indo-1 fluorescence) varied with pace frequency in a similar manner, suggesting that cytoplasmic calcium may play a key role in pace-induced ANF secretion. Furthermore, nifedipine and ryanodine, which inhibited the contractile calcium transients, inhibited pace-induced ANF release, whereas Bay K 8644 increased both the calcium transients and ANF secretion. Pace-induced ANF release was also completely inhibited by KN-62, a specific inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaMK) but was not inhibited by chelerythrine, a protein kinase C-selective inhibitor. Pace-induced ANF release averaged 40% of that elicited by ET which is known to require both PKC and CaMK for maximal effects on ANF secretion. The effects of pacing and ET on ANF secretion were approximately additive. In contrast to pacing, ET strongly stimulated phosphoinositide hydrolysis, activated PKC, and did not increase cytoplasmic calcium. Thus, regulation of ANF secretion by contraction rate depends primarily on the contractile calcium transients and CaMK and is independent of PKC.
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gene expression and atrial natriuretic factor processing and secretion in cultured at 1 cardiac myocytes
Circulation, 1992Co-Authors: Nicholas A Lanson, Christopher C Glembotski, Mark E Steinhelper, Loren J Field, William C ClaycombAbstract:BACKGROUNDStudies were carried out to characterize several biochemical features of cultured AT-1 cells.METHODS AND RESULTSThese cells were obtained from a transplantable atrial cardiomyocyte tumor lineage. Reverse transcriptase-polymerase chain reaction-based analyses demonstrated that the pattern of gene expression of cultured AT-1 cells was similar to that of adult atrial myocytes. AT-1 cells expressed atrial natriuretic factor (ANF), alpha-cardiac myosin heavy chain, alpha-cardiac actin, and connexin43. Radioimmunoassays verified that the cells synthesized, stored, and secreted ANF. Through size-exclusion, reversed-phase, and carboxymethyl-ion-exchange high-performance liquid chromatography, it was shown that cultured AT-1 cells stored ANF as pro-ANF (ANF-[1-126]), which was cosecretionally processed quantitatively to ANF-(1-98) and the bioactive 28-amino-acid ANF-(99-126). In addition, cultured AT-1 cells secreted ANF at almost a sixfold greater rate in response to endothelin-1, a potent secretagogue ...
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the alpha adrenergic stimulation of atrial natriuretic factor expression in cardiac myocytes requires calcium influx protein kinase c and calmodulin regulated pathways
Journal of Biological Chemistry, 1991Co-Authors: C A Sei, C E Irons, Amy B Sprenkle, Patrick M Mcdonough, Joan Heller Brown, Christopher C GlembotskiAbstract:Abstract It has been shown recently that alpha-adrenergic agonists can stimulate atrial natriuretic factor (ANF) expression in ventricular cardiac myocytes; however, little is known about the intracellular signals mediating this activation. The present study focused on the potential roles of calcium-regulated kinases and calcium influx in the alpha-adrenergic stimulation of ANF gene expression in ventricular myocardial cell cultures. Myocardial cells maintained for 48 h in serum-free medium supplemented with phenylephrine (PE) possessed up to 15-fold higher levels of ANF peptide and ANF mRNA than control cells. The removal of PE, or the addition of nifedipine, resulted in a rapid decline in ANF expression, suggesting that the sustained elevation of some intracellular messenger (e.g. calcium and/or phospholipid hydrolysis products) was required for the adrenergic response. The calcium channel agonist BAY K 8644 was capable of increasing ANF expression in a nifedipine-sensitive manner; however, unlike PE, it did not stimulate phosphoinositide hydrolysis. The protein kinase C inhibitor, H7, caused an approximate 75% reduction in PE-stimulated ANF expression, but had no effect on BAY K-stimulated expression. W7, a calcium/calmodulin inhibitor, completely blocked the effects of both PE and BAY K 8644. The addition of either H7 or W7 24 h after the PE addition resulted in a decline of ANF expression. These results indicate that alpha-adrenergic agonists augment ANF gene expression through at least two pathways, one that is H7-sensitive, perhaps involving the sustained activation of protein kinase C, and the other that is W7-sensitive, perhaps involving the sustained activation of calmodulin-regulated kinases. Further, it appears that BAY K 8644-mediated increases in ANF expression are independent of protein kinase C activation and dependent on calmodulin-regulated events.
Bin Yang - One of the best experts on this subject based on the ideXlab platform.
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advanced separators based on aramid nanofiber ANF membranes for lithium ion batteries a review of recent progress
Journal of Materials Chemistry, 2021Co-Authors: Bin Yang, Meiyun Zhang, Lin Wang, Qiankun Zhou, Linxin ZhongAbstract:Lithium-ion batteries (LIBs) have brought great significance and convenience not only in our daily lives, but also in the fields of industrial manufacturing and energy storage. Although the separator is an inactive component in a cell that does not engage in reactions, it has a significant impact on the battery's capacity, cycle performance, and most significantly, its safety and reliability. However, as the need for better safety and reliability, greater energy capacity, faster charge rate, and longer service life grows, conventional commercial polyolefin-based membrane separators often struggle to satisfy the LIB growth requirements and balance the properties of advanced electrode materials. Although great efforts have been made to improve the comprehensive properties of the existing and forthcoming separators, there is not a single separator that can meet all requirements for different battery applications. Considering that aramid nanofiber (ANF)-based membranes have been developed in recent years with superior strength and modulus, excellent thermal stability and unique structure, they have been considered among the most promising candidates for next-generation separators. This review firstly summarizes the requirements and development of high-performance separators, then the characteristics and advantageous properties of ANFs and ANF films are discussed, indicating that the ANF separator will be a promising building block for the next-generation of high-performance LIB separators. Furthermore, the recent application progress and challenges of the ANF-based membrane separators in the classifications of ANF coated separators, pure ANF separators, composite ANF separators, and ANF solid-state electrolytes are summarized and critically discussed, along with a particular focus on the possible strategies to control and regulate the porous structure of the pure ANF separator. The possible challenges and perspectives for the future development of the emerging ANF-based separators are also highlighted.
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comparative study of aramid nanofiber ANF and cellulose nanofiber cnf
Carbohydrate Polymers, 2019Co-Authors: Bin Yang, Meiyun Zhang, Jiaojun Tan, Jingjing Luo, Shunxi Song, Xueyao Ding, Lin Wang, Qiuyu ZhangAbstract:Abstract Cellulose nanofiber (CNF) has faced challenges toward advanced applications due to the poor water resistance, wet strength, and poor thermal stability. The fabrication methods, morphologies and dispersibility between CNF and aramid nanofiber (ANF) were compared. Then the mechanical strength, especially the retention of wet strength (RWS), optical property, UV shielding, wettability and thermal stability of CNF and ANF nanopapers were further investigated. The results show that ANF and ANF nanopaper have significant advantages in dispersibility, water resistance, wet strength, thermal stability and UV-blocking ability over the CNF and CNF nanopaper. Especially the RWS of ANF nanopaper reached ˜82.5%, which notably exceeded the CNF nanopaper of 1.1%. This work demonstrates that the ANF could be an ideal alternative to CNF for advanced nanocomposites. Transparent, flexible, ultra-strong ANF nanopaper with favorable water resistance and wet strength, as well as good UV-blocking property shows great potential in variety of advanced applications.
Rameshwar K Sharma - One of the best experts on this subject based on the ideXlab platform.
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atrial natriuretic factor receptor guanylate cyclase ANF rgc transduces two independent signals ANF and ca2
Frontiers in Molecular Neuroscience, 2014Co-Authors: Teresa Duda, Alexandre Pertzev, Rameshwar K SharmaAbstract:Atrial natriuretic factor receptor guanylate cyclase, ANF-RGC, was the first discovered member of the mammalian membrane guanylate cyclase family. The hallmark feature of the family is that a single protein contains both the site for recognition of the regulatory signal and the ability to transduce it into the production of the second messenger, cyclic GMP. For over two decades, the family has been classified into two subfamilies, the hormone receptor subfamily with ANF-RGC being its paramount member, and the Ca2+ modulated subfamily, which includes the rod outer segment guanylate cyclases, ROS-GC1 and 2, and the olfactory neuroepithelial guanylate cyclase, ONE-GC. ANF-RGC is the receptor and the signal transducer of the most hypotensive hormones, atrial natriuretic factor (ANF) and B-type natriuretic peptide (BNP). After binding these hormones at the extracellular domain it, at its intracellular domain, signals activation of the C-terminal catalytic module and accelerates the production of cyclic GMP. Cyclic GMP then serves the second messenger role in biological responses of ANF and BNP such as natriuresis, diuresis, vasorelaxation and anti-proliferation. Very recently another modus operandi for ANF-RGC was revealed. Its crux is that ANF-RGC activity is also regulated by Ca2+. The Ca2+ sensor neurocalcin mediates this signaling mechanism. Strikingly, the Ca2+ and ANF signaling mechanisms employ separate structural motifs of ANF-RGC in modulating its core catalytic domain in accelerating the production of cyclic GMP. In this review the biochemistry and physiology of these mechanisms with emphasis on cardiovascular regulation will be discussed.
William C Claycomb - One of the best experts on this subject based on the ideXlab platform.
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gene expression and atrial natriuretic factor processing and secretion in cultured at 1 cardiac myocytes
Circulation, 1992Co-Authors: Nicholas A Lanson, Christopher C Glembotski, Mark E Steinhelper, Loren J Field, William C ClaycombAbstract:BACKGROUNDStudies were carried out to characterize several biochemical features of cultured AT-1 cells.METHODS AND RESULTSThese cells were obtained from a transplantable atrial cardiomyocyte tumor lineage. Reverse transcriptase-polymerase chain reaction-based analyses demonstrated that the pattern of gene expression of cultured AT-1 cells was similar to that of adult atrial myocytes. AT-1 cells expressed atrial natriuretic factor (ANF), alpha-cardiac myosin heavy chain, alpha-cardiac actin, and connexin43. Radioimmunoassays verified that the cells synthesized, stored, and secreted ANF. Through size-exclusion, reversed-phase, and carboxymethyl-ion-exchange high-performance liquid chromatography, it was shown that cultured AT-1 cells stored ANF as pro-ANF (ANF-[1-126]), which was cosecretionally processed quantitatively to ANF-(1-98) and the bioactive 28-amino-acid ANF-(99-126). In addition, cultured AT-1 cells secreted ANF at almost a sixfold greater rate in response to endothelin-1, a potent secretagogue ...