Abstract 549: Angiotensin II Attenuates Apelin-36 Release from Human Placental Chorionic Villi

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Liliya M Yamaleyeva ◽  
K. Bridget Brosnihan ◽  
Lauren Anton ◽  
Carolynne McGee ◽  
Heather L Mertz ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Placental Tissue ◽  
Inhibitory Effect ◽  
Negative Influence ◽  
Ang Ii ◽  
Tissue Samples ◽  
Chorionic Villi ◽  
Receptor Localization ◽  
Apelin Receptor ◽  
Human Placental Tissue

Angiotensin II (Ang II) and apelin have opposing actions in the regulation of blood pressure, vascular tone and angiogenesis, factors known to be important in pregnancy. Chorionic villi (CV) are essential for the transport of oxygen and metabolites in the maternal-fetal interface. Previous studies from our group demonstrated the upregulation of Ang II in the CV of preeclamptic women. Since the interaction between Ang II and apelin have been suggested in the cardiovascular system, we determined whether Ang II alters the release of apelin from the placental CV obtained from normotensive pregnant (NP) and preeclamptic (PRE) women. We also established whether Ang-(1-7) influences apelin release from the same set of tissue samples. CV were dissected from the placental tissue, washed and incubated for 0, 2 and 16 hours in DMEM/F12 media with or without Ang II (1 nM and 1 μM) or Ang-(1-7) (1 nM and 1 μM) under controlled O2 and CO2 tensions. The unstimulated release of apelin measured by a competitive radioimmunoassay was significantly reduced in the conditioned media from PRE compared to NP chorionic villi at 2 hrs (PRE: 181.1 ± 31 vs. NP: 309.5 ± 51.4 pg/ml, p<0.05). There was a significant increase in apelin release from both NP (267.8 ± 34.8 vs. baseline: 118.4 ± 27.3 pg/ml, p<0.01) and PRE (293.5 ± 25.8 vs. baseline: 122.6 ± 24.8 pg/ml, p<0.01) CV at 16 hours. Ang II or Ang-(1-7) inhibited the release of apelin from CV of the NP (p<0.05) but not of PRE at 2 hours. At 16 hours, however, Ang II or Ang-(1-7) inhibited the release of apelin from both NP and PRE villi (p<0.05). Immunostaining revealed the predominant localization of apelin receptor to syncytiotrophoblasts and fetal vascular cells of CV - areas associated with AT1 receptor localization. Our data showing a negative influence of Ang II on apelin release from chorionic villi suggest an opposing interaction between these peptides in the human placental tissue. Reduced apelin activity would remove its counter-regulatory actions on Ang II-induced endothelial dysfunction, increased vascular resistance, and inflammation - abnormalities which precede and sustain preeclampsia. A surprising inhibitory effect of Ang-(1-7) on apelin suggests a complex regulation of apelin within the RAS.

Inhibition of angiotensinogen production by angiotensin II analogues in human hepatoma cell line

1989 ◽  
Vol 257 (5) ◽  
pp. C888-C895 ◽  
Author(s):  
E. Coezy ◽  
I. Darby ◽  
J. Mizrahi ◽  
B. Cantau ◽  
M. H. Donnadieu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cell Line ◽  
Binding Sites ◽  
Inhibitory Effect ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Ang Ii ◽  
Hep G2 ◽  
Dose Dependent

The aim of this study was to examine in Hep G2, a human hepatoma-derived cell line, the presence of angiotensin II (ANG II) receptors and the effect of ANG II and its analogues on angiotensinogen production. The presence of ANG II receptors was demonstrated using a long-acting ANG II analogue, 125I-labeled [Sar1]ANG II. A single class of specific binding sites was identified in these cells with a dissociation constant (Kd) of 2 nM. The number and affinity of these binding sites were not changed by [Sar1]ANG II treatment over 24 h. ANG II showed an inhibitory effect on angiotensinogen production. [Sar1]ANG II also exhibited a similar inhibitory effect as that of ANG II but to a greater extent and therefore was used throughout these studies. [Sar1]ANG II inhibited angiotensinogen production in a dose-dependent manner, exhibiting a half-maximal inhibitory concentration (IC50) of 2 nM. Other ANG II analogues showed similar effects on angiotensinogen production. In order of decreasing ability, they were [Sar1]ANG II greater than [Sar1-Ala8]ANG II greater than [Sar1-Val8]ANG II greater than [Sar1-Val5-(Br5)-Phe8]ANG II greater than [Sar1-Val5-DPhe8]ANG II. Results of these studies show that the Hep G2 cell possesses specific ANG II receptors and that [Sar1]ANG II induces a dose-dependent inhibition of angiotensinogen production in this system.

Potentiation of Adrenaline-Induced Platelet Aggregation by Angiotensin II

1985 ◽  
Vol 54 (03) ◽  
pp. 717-720 ◽  
Author(s):  
Yu-An Ding ◽  
D Euan MacIntyre ◽  
Christopher J Kenyon ◽  
Peter F Semple
Keyword(s):  
Platelet Aggregation ◽  
Angiotensin Ii ◽  
Human Platelet ◽  
Inhibitory Effect ◽  
Facilitatory Effect ◽  
Ang Ii ◽  
Human Platelet Aggregation ◽  
Low Concentrations ◽  
High Concentrations ◽  
Stimulation Of

SummaryThe effects of angiotensin II (ANG II) alone and in combination with other agonists on human platelet aggregation, thromboxane B2 (TxB2) and cytosolic [Ca2+]i were investigated. ANG II (10™11 - 10™7 M) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (<2 min) or longterm (30 min) incubation. In contrast, low concentrations of ANG II (10™11 M) enhanced adrenaline-induced platelet aggregation but high concentrations (10™7 M) had an inhibitory effect. Moreover, ANG II (10™11 - 10™7 M) augmented platelet responses to the TxA2 mimetic, U44069. Pretreatment of platelets with flurbiprofen abolished this facilitatory effect of ANG II on adrenaline- but not on U44069-induced platelet aggregation. These results suggest that ANG II stimulation of agonist-induced platelet activation may be due to potentiation of the effects rather than the synthesis of TxA2

scholarly journals Examination of Bcl-2 and Bax Protein Levels for Determining the Apoptotic Changes in Placentas with Gestational Diabetes and Preeclampsia

Proceedings ◽  
2018 ◽  
Vol 2 (25) ◽  
pp. 1548 ◽  
Author(s):  
Ebru Gokalp-Ozkorkmaz ◽  
Firat Asir ◽  
Sureyya Ozdemir Basaran ◽  
Elif Agacayak ◽  
Firat Sahin ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Positive Reaction ◽  
Placental Tissue ◽  
Tissue Samples ◽  
Protein Levels ◽  
Bax Protein ◽  
Protein Expressions ◽  
Human Placental Tissue ◽  
Apoptotic Activity ◽  
Immunohistochemical Techniques

Anti-apoptotic Bcl-2 and proapoptotic Bax genes are the most significant genes that are involved in the regulation of apoptosis. Abnormal apoptotic activity in preeclampsia and gestational diabetes is caused by dysregulation of these genes. In this study; we examined Bcl-2 and Bax protein expressions using immunohistochemical techniques in human placental tissue samples from cases of gestational diabetes (n: 20) and preeclampsia (n: 20). It was observed that Bax expression showed positive reaction compared to Bcl-2 expression so; Bax protein was thought to be an effective marker in determining apoptotic changes in placentas with gestational diabetes and preeclampsia.

Angiotensin II AT2 receptor inhibits smooth muscle cell migration via fibronectin cell production and binding

2002 ◽  
Vol 282 (4) ◽  
pp. C654-C664 ◽  
Author(s):  
Catherine Chassagne ◽  
Christophe Adamy ◽  
Philippe Ratajczak ◽  
Bruno Gingras ◽  
Emmanuel Teiger ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Function ◽  
Cell Attachment ◽  
Smooth Muscle Actin ◽  
Inhibitory Effect ◽  
Receptor Subtype ◽  
Ang Ii

To explore the vascular function of the angiotensin II (ANG II) AT2receptor subtype (AT2R), we generated a vascular smooth muscle cell (SMC) line expressing the AT2R (SMC-vAT2). The involvement of AT2R in the motility response of SMCs was examined in SMC-vAT2 cells and their controls (SMC-v) cultured on either laminin or fibronectin matrix proteins with the agarose drop technique. All experiments were conducted in the presence of a saturating concentration of losartan to inactivate the AT1R subtype. Under basal conditions, both cell lines migrated outside drops, but on laminin only. Treatment with ANG II significantly inhibited the migration of SMC-vAT2but not SMC-v cells, and this effect was prevented by the AT2R antagonist CGP-42112A. The decreased migration of SMC-vAT2 was not associated with changes in cell growth, cytoskeleton stiffness, or smooth muscle actin, desmin, and tenascin expression. However, it was correlated with increased synthesis and binding of fibronectin. Both responses were prevented by incubation with selective AT2R antagonists. Addition of GRGDTP peptide, which prevents cell attachment of fibronectin, reversed the AT2R inhibitory effect on SMC-vAT2 migration. These results suggest that activated ANG II AT2R inhibits SMC migration via cellular fibronectin synthesis and associated cell binding.

Localization of α-interferon in the human feto-placental unit

1988 ◽  
Vol 119 (3) ◽  
pp. 531-NP ◽  
Author(s):  
A. G. Howatson ◽  
M. Farquharson ◽  
A. Meager ◽  
A. M. McNicol ◽  
A. K. Foulis
Keyword(s):  
Biological Effects ◽  
Placental Tissue ◽  
Paraffin Wax ◽  
Immunocytochemical Study ◽  
Chorionic Villi ◽  
Tissue Sections ◽  
Complex Series ◽  
Human Placental Tissue

ABSTRACT The distribution of α-interferon in human placental tissue was investigated by immunocytochemical study of paraffin wax-embedded tissue sections using a sheep α-interferon antiserum. Fifty-eight placentas of gestational ages from 8 to 40 weeks were examined. α-Interferon was present in the syncytiotrophoblast of the chorionic villi of all placentas and was also in macrophages in 28 cases. The appearances suggest production of interferon in human placental trophoblast and, in view of its diverse biological effects, support the concept of a role for α-interferon in the complex series of events required for successful gestation. J. Endocr. (1988) 119, 531–534

Brain angiotensin II tonically modulates sympathetic baroreflex in rabbit ventrolateral medulla

1996 ◽  
Vol 271 (3) ◽  
pp. H1015-H1021 ◽  
Author(s):  
T. Saigusa ◽  
M. Iriki ◽  
J. Arita
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Inhibitory Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Renal Sympathetic

The role of endogenous angiotensin II (ANG II) at the level of the rostral (RVLM) and caudal ventrolateral medulla (CVLM) in the control of sympathetic baroreflex function was investigated in urethan-anesthetized rabbits. The baroreflex relationship between mean arterial pressure and integrated renal sympathetic nerve activity (RSNA) was compared before and during microinfusion of saralasin, an ANG II receptor antagonist into RVLM or CVLM. The infusion of saralasin (20 pmol/min) into RVLM reduced the upper plateau, the range, and the range-dependent gain of the baroreflex, as well as the resting level of RSNA. The infusion of saralasin into CVLM augmented the upper plateau, the reflex range, and the range-dependent gain, whereas it did not alter the resting level of RSNA or mean arterial pressure. These results suggest that 1) the ANG II networks in RVLM are tonically active, influencing the resting level of the sympathetic outflow and facilitating the sympathetic baroreflex function, and 2) the ANG II networks in CVLM do not significantly influence the sympathetic activity in the resting state but exert an inhibitory effect on the baroreflex response when arterial pressure falls below the resting level.

scholarly journals Purification of human procollagen type III N-proteinase from placenta and preparation of antiserum

1986 ◽  
Vol 239 (1) ◽  
pp. 47-52 ◽  
Author(s):  
R Halila ◽  
L Peltonen
Keyword(s):  
Placental Tissue ◽  
Inhibitory Effect ◽  
Affinity Column ◽  
Type I ◽  
Type Iii ◽  
Procollagen Type ◽  
Denatured Protein ◽  
Type Iv ◽  
Human Placental Tissue ◽  
Preparation Of Antiserum

Procollagen type III N-proteinase, of Mr about 70,000, was detected in human placental tissue and purified from this source more than 5800-fold. It was found to be a glycoprotein, which was bound to both concanavalin A-Ultrogel and heparin-Sepharose affinity columns. Binding to a type III pN-collagen-Sepharose affinity column was used as the final step in purification. The purified enzyme accepted only native type III procollagen or [14C]carboxymethylated type III pN-collagen as its substrate; type I, type II and type IV procollagen and heat-denatured type III pN-collagen were not cleaved by the enzyme. Antibodies against this purified enzyme protein raised in rabbits demonstrated a high inhibitory effect on the enzyme activity. Immunoblotting of the denatured protein and immunoelectrophoresis of the native enzyme showed only one major antigenic component, again with an Mr of about 70,000. The antibodies cross-reacted with the enzyme preparation from foetal-calf aorta smooth-muscle cells.

scholarly journals Localized accumulation of angiotensin II and production of angiotensin-(1–7) in rat luteal cells and effects on steroidogenesis

2006 ◽  
Vol 291 (2) ◽  
pp. E221-E233 ◽  
Author(s):  
John R. Pepperell ◽  
Gabor Nemeth ◽  
Yuji Yamada ◽  
Frederick Naftolin ◽  
Maricruz Merino
Keyword(s):  
Angiotensin Ii ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Luteal Cells ◽  
Permeabilized Cells ◽  
Production Studies ◽  
Progesterone Production ◽  
Angiotensin Peptides

These studies aim to investigate subcellular distribution of angiotensin II (ANG II) in rat luteal cells, identify other bioactive angiotensin peptides, and investigate a role for angiotensin peptides in luteal steroidogenesis. Confocal microscopy showed ANG II distributed within the cytoplasm and nuclei of luteal cells. HPLC analysis showed peaks that eluted with the same retention times as ANG-(1–7), ANG II, and ANG III. Their relative concentrations were ANG II ≥ ANG-(1–7) > ANG III, and accumulation was modulated by quinapril, an inhibitor of angiotensin-converting enzyme (ACE), Z-proprolinal (ZPP), an inhibitor of prolyl endopeptidase (PEP), and parachloromercurylsulfonic acid (PCMS), an inhibitor of sulfhydryl protease. Phenylmethylsulfonyl fluoride (PMSF), a serine protease inhibitor, did not affect peptide accumulation. Quinapril, ZPP, PCMS, and PMSF, as well as losartan and PD-123319, the angiotensin receptor type 1 (AT1) and type 2 (AT2) receptor antagonists, were used in progesterone production studies. ZPP significantly reduced luteinizing hormone (LH)-dependent progesterone production ( P < 0.05). Quinapril plus ZPP had a greater inhibitory effect on LH-stimulated progesterone than either inhibitor alone, but this was not reversed by exogenous ANG II or ANG-(1–7). Both PCMS and PMSF acutely blocked LH-stimulated progesterone, and PCMS blocked LH-sensitive cAMP accumulation. Losartan inhibited progesterone production in permeabilized but not intact luteal cells and was reversed by ANG II. PD-123319 had no significant effect on luteal progesterone production in either intact or permeabilized cells. These data suggest that steroidogenesis may be modulated by angiotensin peptides that act in part through intracellular AT1 receptors.

Simplified matrix solid phase dispersion procedure for the determination of parabens and benzophenone-ultraviolet filters in human placental tissue samples

2014 ◽  
Vol 1371 ◽  
pp. 39-47 ◽  
Author(s):  
F. Vela-Soria ◽  
I. Rodríguez ◽  
O. Ballesteros ◽  
A. Zafra-Gómez ◽  
L. Ballesteros ◽  
...  
Keyword(s):  
Solid Phase ◽  
Placental Tissue ◽  
Tissue Samples ◽  
Matrix Solid Phase Dispersion ◽  
Phase Dispersion ◽  
Human Placental Tissue
Sign in / Sign up

Export Citation Format

Share Document