High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.

The objectives of this study were to characterize the effects of plasma lipoproteins on prostacyclin (PGI2) production by the Langendorff-perfused rabbit heart, and to determine the mechanism of lipoprotein-induced cardiac PGI2 production. PGI2 production by perfused rabbit hearts was stimulated by...

Full description

Bibliographic Details
Main Authors: W A Van Sickle, H G Wilcox, K U Malik, A Nasjletti
Format: Article
Language:English
Published: Elsevier 1988-07-01
Series:Journal of Lipid Research
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520351890
_version_ 1818383732759855104
author W A Van Sickle
H G Wilcox
K U Malik
A Nasjletti
author_facet W A Van Sickle
H G Wilcox
K U Malik
A Nasjletti
author_sort W A Van Sickle
collection DOAJ
description The objectives of this study were to characterize the effects of plasma lipoproteins on prostacyclin (PGI2) production by the Langendorff-perfused rabbit heart, and to determine the mechanism of lipoprotein-induced cardiac PGI2 production. PGI2 production by perfused rabbit hearts was stimulated by injections of rabbit very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). HDL was much more effective than equivalent doses of VLDL or LDL. Infusion of HDL at a physiological concentration stimulated cardiac PGI2 output by 417%, but infusion of VLDL or LDL was ineffective. Cardiac PGI2 production increased from 47% to 340% with increasing doses of HDL. The release of cardiac PGI2 in response to injections or infusions of HDL occurred rapidly; maximal release of PGI2 was reached within 2 min after exposure to HDL. Injections of HDL stimulated the production of [3H]arachidonic acid, [3H]prostaglandin E2, [3H]prostaglandin F2 alpha, and [3H]6-keto-prostaglandin F1 alpha from hearts after prelabeling of cardiac lipids with [3H]arachidonic acid. These results indicate that plasma lipoproteins, specifically HDL, stimulate PGI2 production by the isolated rabbit heart. The mechanism by which HDL increases cardiac PGI2 production may involve the mobilization of cardiac arachidonic acid for PGI2 synthesis.
first_indexed 2024-12-14T03:11:03Z
format Article
id doaj.art-7f1e261765ab419b8a30926a235dc602
institution Directory Open Access Journal
issn 0022-2275
language English
last_indexed 2024-12-14T03:11:03Z
publishDate 1988-07-01
publisher Elsevier
record_format Article
series Journal of Lipid Research
spelling doaj.art-7f1e261765ab419b8a30926a235dc6022022-12-21T23:19:16ZengElsevierJournal of Lipid Research0022-22751988-07-01275517522High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.W A Van SickleH G WilcoxK U MalikA NasjlettiThe objectives of this study were to characterize the effects of plasma lipoproteins on prostacyclin (PGI2) production by the Langendorff-perfused rabbit heart, and to determine the mechanism of lipoprotein-induced cardiac PGI2 production. PGI2 production by perfused rabbit hearts was stimulated by injections of rabbit very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). HDL was much more effective than equivalent doses of VLDL or LDL. Infusion of HDL at a physiological concentration stimulated cardiac PGI2 output by 417%, but infusion of VLDL or LDL was ineffective. Cardiac PGI2 production increased from 47% to 340% with increasing doses of HDL. The release of cardiac PGI2 in response to injections or infusions of HDL occurred rapidly; maximal release of PGI2 was reached within 2 min after exposure to HDL. Injections of HDL stimulated the production of [3H]arachidonic acid, [3H]prostaglandin E2, [3H]prostaglandin F2 alpha, and [3H]6-keto-prostaglandin F1 alpha from hearts after prelabeling of cardiac lipids with [3H]arachidonic acid. These results indicate that plasma lipoproteins, specifically HDL, stimulate PGI2 production by the isolated rabbit heart. The mechanism by which HDL increases cardiac PGI2 production may involve the mobilization of cardiac arachidonic acid for PGI2 synthesis.http://www.sciencedirect.com/science/article/pii/S0022227520351890
spellingShingle W A Van Sickle
H G Wilcox
K U Malik
A Nasjletti
High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.
Journal of Lipid Research
title High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.
title_full High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.
title_fullStr High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.
title_full_unstemmed High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.
title_short High density lipoprotein-induced cardiac prostacyclin synthesis in vitro: relationship to cardiac arachidonate mobilization.
title_sort high density lipoprotein induced cardiac prostacyclin synthesis in vitro relationship to cardiac arachidonate mobilization
url http://www.sciencedirect.com/science/article/pii/S0022227520351890
work_keys_str_mv AT wavansickle highdensitylipoproteininducedcardiacprostacyclinsynthesisinvitrorelationshiptocardiacarachidonatemobilization
AT hgwilcox highdensitylipoproteininducedcardiacprostacyclinsynthesisinvitrorelationshiptocardiacarachidonatemobilization
AT kumalik highdensitylipoproteininducedcardiacprostacyclinsynthesisinvitrorelationshiptocardiacarachidonatemobilization
AT anasjletti highdensitylipoproteininducedcardiacprostacyclinsynthesisinvitrorelationshiptocardiacarachidonatemobilization