TLC Characterization of Liposomes Containing Angiotensinogen, Angiotensine I, Angiotensine II and Saralazin

Recent studies have described intracellular binding sites for angiotensine II. In vascular smooth muscle it was found that intracellular injection of angiotensin II increases the Ca2+ level. An alternative method for intracellular delivery of drugs is represented by using liposomes. Thus, the aim of...

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Veröffentlicht in:Biomedical chromatography 1997-05, Vol.11 (3), p.160-163
Hauptverfasser: Brailoiu, Eugen, Todiras, Mihai, Margineanu, Anca, Costuleanu, Marcel, Brailoiu, Cristina, Filipeanu, Catalin, Costuleanu, Angela, Rusu, Valeriu, Petrescu, Gheorghe
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container_end_page 163
container_issue 3
container_start_page 160
container_title Biomedical chromatography
container_volume 11
creator Brailoiu, Eugen
Todiras, Mihai
Margineanu, Anca
Costuleanu, Marcel
Brailoiu, Cristina
Filipeanu, Catalin
Costuleanu, Angela
Rusu, Valeriu
Petrescu, Gheorghe
description Recent studies have described intracellular binding sites for angiotensine II. In vascular smooth muscle it was found that intracellular injection of angiotensin II increases the Ca2+ level. An alternative method for intracellular delivery of drugs is represented by using liposomes. Thus, the aim of this study was to characterize liposomes filled with angiotensinogen, angiotensine I (Ang I), angiotensine II (Ang II), and saralasin by a TLC method and examine the physiological effects of these on rat vascular smooth muscle. Ang II (for all concentrations tested in the aqueous phase) and Ang I (for concentrations less than 10−4 M) did not affect the thin‐layer chromatography migration of this type of vesicle, suggesting that dose‐dependent effects on physio‐pharmacological experiments could be studied. On the other hand, this type of experiment could not be performed for salarasin‐ or angiotensinogen‐filled liposomes. Administration of liposomes containing Ang II (10−6 M), Ang I (10−6 M), angiotensinogen (10−6 M) and saralasine (10−6 M) caused the contraction to isolated rat aorta smooth muscle, suggesting the presence of active intracellular binding sites. © 1997 John Wiley & Sons, Ltd.
doi_str_mv 10.1002/(SICI)1099-0801(199705)11:3<160::AID-BMC661>3.0.CO;2-T
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In vascular smooth muscle it was found that intracellular injection of angiotensin II increases the Ca2+ level. An alternative method for intracellular delivery of drugs is represented by using liposomes. Thus, the aim of this study was to characterize liposomes filled with angiotensinogen, angiotensine I (Ang I), angiotensine II (Ang II), and saralasin by a TLC method and examine the physiological effects of these on rat vascular smooth muscle. Ang II (for all concentrations tested in the aqueous phase) and Ang I (for concentrations less than 10−4 M) did not affect the thin‐layer chromatography migration of this type of vesicle, suggesting that dose‐dependent effects on physio‐pharmacological experiments could be studied. On the other hand, this type of experiment could not be performed for salarasin‐ or angiotensinogen‐filled liposomes. 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Chromatogr</addtitle><description>Recent studies have described intracellular binding sites for angiotensine II. In vascular smooth muscle it was found that intracellular injection of angiotensin II increases the Ca2+ level. An alternative method for intracellular delivery of drugs is represented by using liposomes. Thus, the aim of this study was to characterize liposomes filled with angiotensinogen, angiotensine I (Ang I), angiotensine II (Ang II), and saralasin by a TLC method and examine the physiological effects of these on rat vascular smooth muscle. Ang II (for all concentrations tested in the aqueous phase) and Ang I (for concentrations less than 10−4 M) did not affect the thin‐layer chromatography migration of this type of vesicle, suggesting that dose‐dependent effects on physio‐pharmacological experiments could be studied. On the other hand, this type of experiment could not be performed for salarasin‐ or angiotensinogen‐filled liposomes. 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Ang II (for all concentrations tested in the aqueous phase) and Ang I (for concentrations less than 10−4 M) did not affect the thin‐layer chromatography migration of this type of vesicle, suggesting that dose‐dependent effects on physio‐pharmacological experiments could be studied. On the other hand, this type of experiment could not be performed for salarasin‐ or angiotensinogen‐filled liposomes. Administration of liposomes containing Ang II (10−6 M), Ang I (10−6 M), angiotensinogen (10−6 M) and saralasine (10−6 M) caused the contraction to isolated rat aorta smooth muscle, suggesting the presence of active intracellular binding sites. © 1997 John Wiley &amp; Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley &amp; Sons, Ltd</pub><pmid>9192109</pmid><doi>10.1002/(SICI)1099-0801(199705)11:3&lt;160::AID-BMC661&gt;3.0.CO;2-T</doi><tpages>4</tpages></addata></record>
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subjects angiotensime I
angiotensime II
Angiotensin I - analysis
Angiotensin II - analysis
Angiotensin-Converting Enzyme Inhibitors - analysis
angiotensinogen
Angiotensinogen - analysis
Angiotensins - analysis
Animals
Chromatography, Thin Layer - methods
liposomes
Liposomes - chemistry
Male
Rats
Rats, Wistar
Saralasin - analysis
TLC
vascular smooth muscle
title TLC Characterization of Liposomes Containing Angiotensinogen, Angiotensine I, Angiotensine II and Saralazin
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