Mechanisms of Action of Atrial Natriuretic Factor and C-Type Natriuretic Peptide

Hypertension ◽  
1996 ◽  
Vol 27 (3) ◽  
pp. 684-687 ◽  
Author(s):  
Janki Amin ◽  
Oscar A. Carretero ◽  
Sadayoshi Ito
Keyword(s):  
Natriuretic Peptide ◽  
Atrial Natriuretic Factor ◽  
Mechanisms Of Action ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Evidence for Atrial Natriuretic Factor Induced Natriuretic Peptide Receptor Subtype Switching in Rat Proximal Tubular Cells during Culture

1998 ◽  
Vol 6 (2) ◽  
pp. 104-111 ◽  
Author(s):  
Sanjay K. Mistry ◽  
Prabal K. Chatterjee ◽  
Roshan P. Weerackody ◽  
Gabrielle M. Hawksworth ◽  
Rachel M. Knott ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Atrial Natriuretic Factor ◽  
Receptor Subtype ◽  
Natriuretic Peptide Receptor ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Peptide Receptor ◽  
Natriuretic Factor ◽  
Proximal Tubular ◽  
Atrial Natriuretic

scholarly journals Atrial natriuretic factor and C-type natriuretic peptide induce retraction of human thyrocytes in monolayer culture via guanylyl cyclase receptors

2002 ◽  
Vol 173 (1) ◽  
pp. 169-176 ◽  
Author(s):  
DF Sellitti ◽  
C Lagranha ◽  
G Perrella ◽  
F Curcio ◽  
SQ Doi
Keyword(s):  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Atrial Natriuretic Factor ◽  
Kinase Inhibitor ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Receptor Subtypes ◽  
Natriuretic Factor ◽  
Human Thyroid Cell ◽  
Atrial Natriuretic

The natriuretic peptides signal through three receptor subtypes, of which two (NPR-A and NPR-B) are membrane-bound guanylyl cyclases for which the principal ligands are respectively atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP). In the human thyroid cell, a third receptor, NPR-C, has been implicated in the regulation of thyroglobulin, but functional roles for NPR-A and NPR-B have not yet been defined. In the present study we used RT-PCR to identify transcripts of all three receptor subtypes, both in human thyroid and in HTU-5 cells, a long-term culture of thyroid-derived cells. Both ANF and CNP induced a twofold increase in intracellular cGMP content in HTU-5 cells. Morphologic changes (a significant increase in cells of the retracted phenotype) were observed in ANF- and CNP-treated cells within 3 and 5 h of treatment respectively. Significant increases in retracted cell number were induced by ANF and CNP, but not the NPR-C-specific ring-deleted ANF analog, C-ANF(4-23), during a 15-day treatment. All three natriuretic peptides, however, induced a small (15-20%) but significant (P<0 small middle dot001) increase in DNA content per well. The stable analog of cGMP, 8-bromo-cGMP (8-BrcGMP; 1 mM), also increased the number of retracted HTU-5 cells, and was equipotent with the cAMP analog, 8-BrcAMP, in this effect. The cGMP-dependent protein kinase inhibitor, KT5823, however, had no significant effect on the ANF-induced increase in numbers of retracted cells. These results suggest that the actions of NPR-A and NPR-B, functional receptors in the human thyroid cell, may in part be mediated by cGMP-induced alterations in the cytoskeleton.

The expression and secretion of atrial natriuretic factor and brain natriuretic peptide by rat proximal tubular cells

2000 ◽  
Vol 59 (7) ◽  
pp. 783-790 ◽  
Author(s):  
Sanjay Mistry ◽  
Benedict Lussert ◽  
Keith Stewart ◽  
Gabrielle M Hawksworth ◽  
Alan Struthers ◽  
...  
Keyword(s):  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic Factor ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Natriuretic Factor ◽  
Proximal Tubular ◽  
Atrial Natriuretic

Atrial natriuretic factor binding sites in rat area postrema: autoradiographic study

1992 ◽  
Vol 263 (4) ◽  
pp. R747-R755 ◽  
Author(s):  
E. M. Konrad ◽  
G. Thibault ◽  
E. L. Schiffrin
Keyword(s):  
Natriuretic Peptide ◽  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Cellular Localization ◽  
Area Postrema ◽  
Receptor Subtype ◽  
Electron Microscopic ◽  
Electron Microscopic Autoradiography ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The area postrema (AP) is a brain stem circumventricular organ implicated, among other functions, in central cardiovascular (CV) regulation. Competition binding analysis performed by quantitative in vitro autoradiography demonstrated specific, high-affinity (Kd, 0.32 +/- 0.11 nM), low-capacity (Bmax, 57.5 +/- 10.9 fmol/mg protein) atrial natriuretic factor (ANF) binding sites in the AP. C-ANF [des-(Gln116-Gly120)ANF-(Arg102-Cys121)-NH2] and ANF-(Phe106-Ile113)-NH2 (two ligands endowed with selectivity for the ANF-C receptor), as well as C-type natriuretic peptide (CNP), did not compete noticeably at pathophysiological concentrations for 125I-ANF binding. 125I-[Tyr0]CNP bound to the AP to a much lower extent than 125I-ANF. Electron microscopic autoradiography in vivo disclosed that 125I-ANF was preferentially bound to axon, dendrite, and astrocyte plasmalemma. These studies demonstrate that the AP contains natriuretic peptide binding sites with pharmacological characteristics of the ANF-A and ANF-B but not of the ANF-C receptor subtype. In the AP, ANF interacts with those sites resembling ANF-A receptors. Cellular localization of these binding sites may relate to their possible involvement in the centrally mediated salt and water regulation and/or CV effects of circulating ANF.

scholarly journals Differential effects of rat pregnancy on uterine and lung atrial natriuretic factor receptors

1998 ◽  
Vol 274 (1) ◽  
pp. E52-E56 ◽  
Author(s):  
Patrice Vaillancourt ◽  
Saeed Omer ◽  
Xing-Fei Deng ◽  
Shree Mulay ◽  
Daya R. Varma
Keyword(s):  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Atrial Natriuretic Factor ◽  
Receptor Protein ◽  
Differential Effects ◽  
Natriuretic Factor ◽  
Organ Specific ◽  
Atrial Natriuretic

We investigated if the refractoriness to the tocolytic effects of atrial natriuretic factor (ANF) during rat pregnancy is due to a downregulation of one or both guanylyl cyclase (GC)-coupled GC-A and GC-B ANF receptors; lungs were used as controls. Uteri and lungs of virgin, pregnant ( days 7, 16, and 21), and day 2postpartum rats expressed mRNAs for GC-A and GC-B as well as GC-uncoupled ANF-C receptors. GC-B receptor protein was more abundant than GC-A in uteri; the reverse was the case in lungs. Pregnancy decreased uterine mRNAs and proteins for GC-A and GC-B receptors as well as the effects of ANF and C-type natriuretic peptide (CNP) on uterine GC activity; lung ANF receptors and effects of ANF and CNP on lung GC activity were not modulated by pregnancy. It is concluded that pregnancy induces organ-specific modulation of ANF receptors and a downregulation of ANF-GC receptors would minimize interference with uterine motility during pregnancy.

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