Basal and PGE2-stimulated duodenal bicarbonate secretion in the rat in vivo

1988 ◽  
Vol 255 (4) ◽  
pp. G470-G475 ◽  
Author(s):  
J. R. Heylings ◽  
M. Feldman
Keyword(s):  
Prostaglandin E2 ◽  
Intravenous Administration ◽  
Concentration Gradient ◽  
Bicarbonate Secretion ◽  
Dependent Process ◽  
Duodenal Bicarbonate Secretion ◽  
Presence And Absence ◽  
Energy Dependent

We studied basal and prostaglandin E2 (PGE2)-stimulated duodenal HCO3- transport in the rat in vivo both in the presence and absence of a concentration gradient for HCO3- from blood to lumen. Basal HCO3- transport was not reduced when the luminal solution was changed from one containing 0 mM HCO3- to one containing 22 mM HCO3- either at pH 9.0 or 7.5. Thus basal duodenal HCO3- transport in rats is independent of a blood-to-lumen HCO3- concentration gradient, which indicates an energy-dependent process with little passive flux of HCO3-. Luminal or intravenous administration of PGE2 significantly (P less than 0.01) increased HCO3- secretion into a HCO3(-)-free luminal solution but had no effect on HCO3- secretion into luminal solutions containing 22 mM HCO3-, either at pH 9.0 or 7.5. Therefore prostaglandins may act by increasing passive flux of HCO3- rather than by stimulating energy-dependent duodenal HCO3- transport.

Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion

1989 ◽  
Vol 256 (5) ◽  
pp. G833-G836 ◽  
Author(s):  
M. C. Algazi ◽  
H. S. Chen ◽  
M. A. Koss ◽  
D. L. Hogan ◽  
J. Steinbach ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Vasoactive Intestinal Peptide ◽  
Bicarbonate Secretion ◽  
Anesthetized Rats ◽  
Duodenal Bicarbonate Secretion ◽  
Presence And Absence

Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. In anesthetized rats, the effects of intravenous VIP, intraluminal PGE2, and intraluminal HCl on duodenal mucosal bicarbonate secretion both in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were measured. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. These findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP.

The role of SLC26A6 and CFTR in acid-induced and prostaglandin E2-stimulated duodenal bicarbonate secretion in vivo

2007 ◽  
Vol 45 (08) ◽  
Author(s):  
A Singh ◽  
M Sjöblom ◽  
A Krabbenhöft ◽  
B Riederer ◽  
MP Manns ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Bicarbonate Secretion ◽  
Duodenal Bicarbonate Secretion

TRH-induced vagal stimulation of duodenal HCO-3 mediated by VIP and muscarinic pathways

1989 ◽  
Vol 257 (5) ◽  
pp. G677-G682 ◽  
Author(s):  
H. J. Lenz ◽  
W. W. Vale ◽  
J. E. Rivier
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intravenous Administration ◽  
Vagal Stimulation ◽  
Bicarbonate Secretion ◽  
Endogenous Opiates ◽  
Duodenal Bicarbonate Secretion ◽  
The Central Nervous System ◽  
Freely Moving ◽  
Stimulation Of

The central nervous system effects of thyrotropin-releasing hormone (TRH) on proximal duodenal bicarbonate secretion were studied in freely moving rats. Cerebroventricular administration of TRH (0.5-5.0 nmol) significantly stimulated basal duodenal bicarbonate secretion, whereas intravenous administration of TRH did not. Ganglionic blockade with chlorisondamine and truncal vagotomy abolished TRH-induced bicarbonate secretion, whereas atropine significantly attenuated the response. The vasoactive intestinal peptide (VIP) receptor antagonist, (4Cl-D-Phe6, Leu17) VIP given intravenously completely prevented the stimulatory effect of central TRH on duodenal bicarbonate secretion. In contrast, hypophysectomy, adrenalectomy, opiate and noradrenergic blockade, or indomethacin did not affect the TRH-induced bicarbonate response. Intravenous administration of VIP and carbachol significantly stimulated bicarbonate outputs, and these responses were blocked by the VIP antagonist and atropine, respectively. These results indicate that TRH may serve as a central nervous system mediator that stimulates duodenal bicarbonate secretion in rats by increasing vagal outflow. Vagal stimulation induced by TRH increases duodenal bicarbonate secretion by the release of VIP and, in part, by activation of a muscarinic pathway but not by pituitary, adrenal, and noradrenergic pathways or endogenous opiates and prostaglandins. The actions of peripheral VIP and carbachol appear to be mediated by specific VIP and muscarinic receptors, respectively.

Anion transport pathways involved in PG E2 and acid-stimulated murine duodenal bicarbonate secretion in vivo

2006 ◽  
Vol 44 (08) ◽  
Author(s):  
A Singh ◽  
A Krabbenhöft ◽  
B Riederer ◽  
M Manns ◽  
M Soleimani ◽  
...  
Keyword(s):  
Anion Transport ◽  
Bicarbonate Secretion ◽  
Transport Pathways ◽  
Duodenal Bicarbonate Secretion ◽  
Pg E2

scholarly journals Is Protein Folding a Thermodynamically Unfavorable, Active, Energy-Dependent Process?

2022 ◽  
Vol 23 (1) ◽  
pp. 521
Author(s):  
Irina Sorokina ◽  
Arcady R. Mushegian ◽  
Eugene V. Koonin
Keyword(s):  
Free Energy ◽  
Protein Folding ◽  
Structure Prediction ◽  
Alternative View ◽  
Current View ◽  
Translation System ◽  
Small Proteins ◽  
Dependent Process ◽  
Energy Dependent

The prevailing current view of protein folding is the thermodynamic hypothesis, under which the native folded conformation of a protein corresponds to the global minimum of Gibbs free energy G. We question this concept and show that the empirical evidence behind the thermodynamic hypothesis of folding is far from strong. Furthermore, physical theory-based approaches to the prediction of protein folds and their folding pathways so far have invariably failed except for some very small proteins, despite decades of intensive theory development and the enormous increase of computer power. The recent spectacular successes in protein structure prediction owe to evolutionary modeling of amino acid sequence substitutions enhanced by deep learning methods, but even these breakthroughs provide no information on the protein folding mechanisms and pathways. We discuss an alternative view of protein folding, under which the native state of most proteins does not occupy the global free energy minimum, but rather, a local minimum on a fluctuating free energy landscape. We further argue that ΔG of folding is likely to be positive for the majority of proteins, which therefore fold into their native conformations only through interactions with the energy-dependent molecular machinery of living cells, in particular, the translation system and chaperones. Accordingly, protein folding should be modeled as it occurs in vivo, that is, as a non-equilibrium, active, energy-dependent process.

scholarly journals Dual roles for ATP in the regulation of phase separated protein aggregates in Xenopus oocyte nucleoli

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Michael H Hayes ◽  
Elizabeth H Peuchen ◽  
Norman J Dovichi ◽  
Daniel L Weeks
Keyword(s):  
Adenosine Triphosphate ◽  
Xenopus Oocyte ◽  
Protein Solubility ◽  
Protein Aggregates ◽  
Dual Roles ◽  
Dependent Process ◽  
Nuclear Factors ◽  
Energy Dependent

For many proteins, aggregation is one part of a structural equilibrium that can occur. Balancing productive aggregation versus pathogenic aggregation that leads to toxicity is critical and known to involve adenosine triphosphate (ATP) dependent action of chaperones and disaggregases. Recently a second activity of ATP was identified, that of a hydrotrope which, independent of hydrolysis, was sufficient to solubilize aggregated proteins in vitro. This novel function of ATP was postulated to help regulate proteostasis in vivo. We tested this hypothesis on aggregates found in Xenopus oocyte nucleoli. Our results indicate that ATP has dual roles in the maintenance of protein solubility. We provide evidence of endogenous hydrotropic action of ATP but show that hydrotropic solubilization of nucleolar aggregates is preceded by a destabilizing event. Destabilization is accomplished through an energy dependent process, reliant upon ATP and one or more soluble nuclear factors, or by disruption of a co-aggregate like RNA.

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