Human placental acetylcholine

1991 ◽  
Vol 3 (4) ◽  
pp. 405 ◽  
Author(s):  
RG King ◽  
NM Gude ◽  
BR Krishna ◽  
S Chen ◽  
SP Brennecke ◽  
...  
Keyword(s):  
Blood Flow ◽  
Amino Acid ◽  
Cholinergic System ◽  
Vascular Tone ◽  
Perfusion Pressure ◽  
Acid Transport ◽  
Ach Release ◽  
Fetal Vessels

The human placenta contains both acetylcholine (ACh) and choline acetyltransferase, and in vitro bilaterally perfused placental lobules release ACh. The function of this placental cholinergic system has not yet been clearly defined, although changes occur in it during parturition and it may be linked to placental prostaglandin generation at this time. It has also been suggested that ACh may regulate placental amino-acid transport and/or blood flow. It has been found that ACh release from fetal vessels of bilaterally perfused placental lobules is reduced during preeclampsia but is not necessarily correlated with any change in perfusion pressure or materno-fetal transfer of the nonmetabolizable amino acid alpha-aminoisobutyric acid. However, a correlation has been found between releases from human placental explants of ACh (when inhibited by (2-benzoylethyl)trimethylammonium or vesamicol) and of prostaglandins E2 and F2 alpha. Thus, although the evidence for a role of ACh in the control of placental amino-acid transfer or vascular tone is not conclusive, inhibition of the human placental cholinergic system has been shown to be associated with reduced output of prostaglandins from this tissue.

Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow

1994 ◽  
Vol 266 (2) ◽  
pp. F275-F282 ◽  
Author(s):  
A. P. Zou ◽  
J. D. Imig ◽  
M. Kaldunski ◽  
P. R. Ortiz de Montellano ◽  
Z. Sui ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Epoxyeicosatrienoic Acids ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Renal Vascular

The present study evaluated the role of endogenous P-450 metabolites of arachidonic acid (AA) on autoregulation of renal blood flow in rats. Whole kidney and cortical blood flows were well autoregulated when renal perfusion pressure was varied from 150 to 100 mmHg. Infusion of 17-octadecynoic acid (17-ODYA) into the renal artery (33 nmol/min) increased cortical and papillary blood flows by 12.6 +/- 2.5 and 26.5 +/- 4.6%, respectively. After 17-ODYA, autoregulation of whole kidney and cortical blood flows was impaired. Intrarenal infusion of miconazole (8 nmol/min) had no effect on autoregulation of whole kidney, cortical, or papillary blood flows. 17-ODYA (1 microM) inhibited the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) and 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) by renal preglomerular microvessels in vitro by 83.7 +/- 7.4% and 89.0 +/- 4.9%, respectively. Miconazole (1 microM) reduced the formation of EETs by 86.4 +/- 5.7%, but it had no effect on the production of 20-HETE. These results suggest that endogenous P-450 metabolites of AA, particularly 20-HETE, may participate in the autoregulation of renal blood flow.

The Role of Energy Metabolism in the Interaction between Amino Acid and Sugar Transport in the Small Intestine

1973 ◽  
Vol 51 (5) ◽  
pp. 378-382 ◽  
Author(s):  
I. Bihler ◽  
P. C. Sawh
Keyword(s):  
Amino Acid ◽  
Energy Metabolism ◽  
Sugar Transport ◽  
Intestinal Transport ◽  
Metabolic Energy ◽  
Acid Transport ◽  
Limited Supply ◽  
Everted Sacs

The interaction between sugar and amino acid transport was studied in everted sacs of rat jejunum in vitro. The addition of the actively transported nonmetabolized sugars, D-galactose and α-methyl-D-glucoside, to the mucosal medium inhibited the active transport of cycloleucine (1-amino-cyclopentane-1-carboxylic acid). This effect was largely counteracted by the simultaneous presence of D-glucose in the serosal medium or of D-fructose. The results indicate that provision of substrates for energy metabolism relieves the inhibition of transport and supports the hypothesis that the interaction between the intestinal transport of sugar and of amino acid is at least in part due to competition for a limited supply of metabolic energy.

scholarly journals Specificity of the HIV-1 Protease on Substrates Representing the Cleavage Site in the Proximal Zinc-Finger of HIV-1 Nucleocapsid Protein

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1092
Author(s):  
János András Mótyán ◽  
Márió Miczi ◽  
Stephen Oroszlan ◽  
József Tőzsér
Keyword(s):  
Amino Acid ◽  
Zinc Finger ◽  
Cleavage Site ◽  
Potential Role ◽  
Binding Mode ◽  
Interaction Energies ◽  
Vitro Assay ◽  
Hiv 1

To explore the sequence context-dependent nature of the human immunodeficiency virus type 1 (HIV-1) protease’s specificity and to provide a rationale for viral mutagenesis to study the potential role of the nucleocapsid (NC) processing in HIV-1 replication, synthetic oligopeptide substrates representing the wild-type and modified versions of the proximal cleavage site of HIV-1 NC were assayed as substrates of the HIV-1 protease (PR). The S1′ substrate binding site of HIV-1 PR was studied by an in vitro assay using KIVKCF↓NCGK decapeptides having amino acid substitutions of N17 residue of the cleavage site of the first zinc-finger domain, and in silico calculations were also performed to investigate amino acid preferences of S1′ site. Second site substitutions have also been designed to produce “revertant” substrates and convert a non-hydrolysable sequence (having glycine in place of N17) to a substrate. The specificity constants obtained for peptides containing non-charged P1′ substitutions correlated well with the residue volume, while the correlation with the calculated interaction energies showed the importance of hydrophobicity: interaction energies with polar residues were related to substantially lower specificity constants. Cleavable “revertants” showed one residue shift of cleavage position due to an alternative productive binding mode, and surprisingly, a double cleavage of a substrate was also observed. The results revealed the importance of alternative binding possibilities of substrates into the HIV-1 PR. The introduction of the “revertant” mutations into infectious virus clones may provide further insights into the potential role of NC processing in the early phase of the viral life-cycle.

Role of cysteine in jaundice hemorrhages

1935 ◽  
Vol 31 (8-9) ◽  
pp. 1114-1114
Keyword(s):  
Amino Acid ◽  
Obstructive Jaundice ◽  
Blood Clotting ◽  
In Vitro Experiments ◽  
Main Factor

The role of calcium, platelets, and other factors that were associated with bleeding was not confirmed in jaundice. Carr and Toote found that the amino acid cysteine was the main factor impeding blood clotting. In obstructive jaundice, this amino acid accumulates in the blood and in in vitro experiments and, when administered to animals, causes a deterioration in blood clotting.

Modulation of vascular tone in renal microcirculation by erythrocytes: role of EDRF

1993 ◽  
Vol 264 (1) ◽  
pp. H190-H195 ◽  
Author(s):  
J. D. Imig ◽  
D. Gebremedhin ◽  
D. R. Harder ◽  
R. J. Roman
Keyword(s):  
Vascular Tone ◽  
Physiological Salt Solution ◽  
Nitric Oxide Synthase Inhibitor ◽  
Renal Microcirculation ◽  
Vasoconstrictor Response ◽  
A Cell ◽  
Afferent Arterioles ◽  
Synthase Inhibitor

The effect of erythrocytes (red blood cells, RBC) on vascular tone in the renal microcirculation was examined using the juxtamedullary nephron microvascular preparation perfused in vitro with a physiological salt solution containing 5% albumin. The basal diameters of the arcuate, interlobular, proximal, and distal afferent arterioles averaged 444 +/- 24, 74 +/- 3, 29 +/- 1, and 19 +/- 1 micron, respectively, when perfused with a cell-free solution at a pressure of 80 mmHg. The diameters of the arcuate and interlobular arteries increased by 14 +/- 4 and 13 +/- 4%, respectively, whereas the diameter of the proximal and distal portions of the afferent arterioles decreased by 7 +/- 2% when perfusion pressure was elevated from 80 to 160 mmHg. The addition of RBC to the perfusate reduced the basal diameters of interlobular and afferent arterioles by 11 +/- 4 and 15 +/- 3%, respectively. The maximal vasoconstrictor response was seen after the addition of only 1% RBC to the perfusate. Removal of platelets did not block the vasoconstrictor response to addition of RBC to the perfusate. The role of endothelium-derived relaxing factor (EDRF) in the vasoconstrictor response to RBC was studied by addition of nitric oxide synthase inhibitor, N omega-nitro-L-arginine (L-NNA, 100 microM) to the perfusate. L-NNA reduced the basal diameters of interlobular and afferent arterioles by 7 +/- 3 and 9 +/- 3%, respectively, and abolished the vasoconstrictor response to RBC. L-NNA had no effect on the pressure-diameter relationships of the preglomerular vasculature when added to perfusates already containing RBC.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Antagonists of the system L neutral amino acid transporter (LAT) promote endothelial adhesivity of human red blood cells

2017 ◽  
Vol 117 (07) ◽  
pp. 1402-1411 ◽  
Author(s):  
Laura Beth Mann Dosier ◽  
Vikram J. Premkumar ◽  
Hongmei Zhu ◽  
Izzet Akosman ◽  
Michael F. Wempe ◽  
...  
Keyword(s):  
Amino Acid ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Amino Acid Transporter ◽  
Neutral Amino Acid ◽  
Neutral Amino Acid Transporter ◽  
System L

SummaryThe system L neutral amino acid transporter (LAT; LAT1, LAT2, LAT3, or LAT4) has multiple functions in human biology, including the cellular import of S-nitrosothiols (SNOs), biologically active derivatives of nitric oxide (NO). SNO formation by haemoglobin within red blood cells (RBC) has been studied, but the conduit whereby a SNO leaves the RBC remains unidentified. Here we hypothesised that SNO export by RBCs may also depend on LAT activity, and investigated the role of RBC LAT in modulating SNO-sensitive RBC-endothelial cell (EC) adhesion. We used multiple pharmacologic inhibitors of LAT in vitro and in vivo to test the role of LAT in SNO export from RBCs and in thereby modulating RBC-EC adhesion. Inhibition of human RBC LAT by type-1-specific or nonspecific LAT antagonists increased RBC-endothelial adhesivity in vitro, and LAT inhibitors tended to increase post-transfusion RBC sequestration in the lung and decreased oxygenation in vivo. A LAT1-specific inhibitor attenuated SNO export from RBCs, and we demonstrated LAT1 in RBC membranes and LAT1 mRNA in reticulocytes. The proadhesive effects of inhibiting LAT1 could be overcome by supplemental L-CSNO (S-nitroso-L-cysteine), but not D-CSNO or L-Cys, and suggest a basal anti-adhesive role for stereospecific intercellular SNO transport. This study reveals for the first time a novel role of LAT1 in the export of SNOs from RBCs to prevent their adhesion to ECs. The findings have implications for the mechanisms of intercellular SNO signalling, and for thrombosis, sickle cell disease, and post-storage RBC transfusion, when RBC adhesivity is increased.

scholarly journals Role of Perfusion Pressure in Major Organ Blood Flow during Cardiopulmonary Bypass in Canines

2000 ◽  
Vol 39 (5) ◽  
pp. 748
Author(s):  
Young Lan Kwak ◽  
Young Hwan Park ◽  
Sang Beom Nam ◽  
Young Jun Oh ◽  
Seung Ho Kim ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Perfusion Pressure ◽  
Organ Blood Flow ◽  
Major Organ

scholarly journals Neuroprotective effect of secretin in chronic hypoxia induced neurodegeneration in rats

2017 ◽  
Vol 6 (2) ◽  
pp. 298
Author(s):  
Gowtham Padmanaban ◽  
M. K. Kayalvizhi ◽  
Kalyanasundaram Kasiviswanathan ◽  
Ruckmani Arunachalam ◽  
Vishnu Kumar Urkavalan
Keyword(s):  
Blood Flow ◽  
Amino Acid ◽  
Experimental Design ◽  
Rat Model ◽  
Chronic Hypoxia ◽  
Neuroprotective Effect ◽  
Proper Functioning ◽  
Partial Pressures

Background: Hypoxia is a condition in any stage in the delivery of oxygen to cells which include decreased partial pressures of oxygen, less diffusion of oxygen in the lungs, insufficient hemoglobin, inefficient blood flow to the end tissue, and breathing rhythm. Secretin is an amino acid which plays proper functioning of gastro intestinal system.Methods: The current study was conducted to evaluvate the effect of exogenously administrated secretin on chronic hypoxic damage of brain in rat model. Experimental design consists of control animals, Control animals + secretin hypoxia exposed animals; hypoxia exposed animals +secretin (20ng/kg.bw).Results: The results of this study point to a possible role of Secretin as neuroprotectant.Conclusions: Further research on secretin needs to be conducted in order to confirm the deductions made by this study.

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