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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.
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.
Teresa Duda - 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.
Andrew F Russo - One of the best experts on this subject based on the ideXlab platform.
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cell specific activation of the atrial Natriuretic Factor promoter by pitx2 and mef2a
Journal of Biological Chemistry, 2004Co-Authors: Rafael Toro, Mona Nemer, Irfan Saadi, Adisa Kuburas, Andrew F RussoAbstract:The PITX2 homeodomain protein is mutated in patients with Axenfeld-Rieger syndrome and is involved in the development of multiple organ systems, including the heart. We have examined the interaction of PITX2 isoforms with myocyte-enhancing Factor 2A (MEF2A), which is a known regulator of cardiac development. A direct interaction between PITX2a and MEF2A was demonstrated using yeast two-hybrid and GST pull-down assays. To study the functional significance of this interaction, we used the atrial Natriuretic Factor (ANF) promoter. Coexpression of MEF2A and PITX2a or Pitx2c resulted in a strong synergistic activation of the ANF promoter in LS8 oral epithelial cells but not in other cell lines (NIH/3T3, Chinese hamster ovary, or C2C12). The synergism was dependent on promoter context, because it required MEF2 binding sites and was not seen with two other PITX2 target promoters. DNA binding by MEF2A was required but not sufficient for synergism. Upstream activators of p38 MAP kinases, MKK3 and MKK6, increased PITX2a and Pitx2c activity to yield up to 90-fold activation of the ANF promoter in LS8 cells. Because Axenfeld-Rieger syndrome is autosomal dominant and affects development of the oral epithelium, we tested one of the known PITX2 mutants. The PITX2a-K88E mutant protein suppressed wild type PITX2a synergism with MEF2A. These results demonstrate a promoter- and cell-specific functional interaction between PITX2 and MEF2A and suggest the possibility of coordinate control by these Factors in the oral epithelium.
Alexandre Pertzev - 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.