Abstract
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.
Highlights
The objectives of this study were to characterize the effects of plasma lipoproteins on prostacyclin (PGIp)production by the Langendorff-perfused rabbit heart, and to determine the mechanism of lipoprotein-induced cardiac PG12 production
Our data demonstrate that high density lipoproteins (HDL) stimulates the production of PGIp by the isolated, perfused rabbit heart, We cannot identify the type of cell that is affected by HDL, this result is consistent with other reports of a stimulatory effect of HDL on PG12synthesis by cultured vascular cells [1,2,3] and on the conversion of the prostaglandin endoperoxide, PGH2, to PG12 by aortic microsomes [11]
We found that very low density lipoproteins (VLDL) and low density lipoproteins (LDL) stimulated cardiac PGIp synthesis, but at equivalent doses of cholesterol were less effective than HDL
Summary
The objectives of this study were to characterize the effects of plasma lipoproteins on prostacyclin (PGIp)production by the Langendorff-perfused rabbit heart, and to determine the mechanism of lipoprotein-induced cardiac PG12 production. PGIp 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). These results indicate that plasma lipoproteins, HDL, stimulate PGIz production by the isolated rabbit heart. The mechanism by which HDL increases cardiac PGIpproduction may involve the mobilization of cardiac arachidonic acid for PGIp synthesis. It has been suggested that HDL delivers arachidonic acid to cultured vascular smooth muscle cells, and thereby stimulates prostaglandin synthesis [1]. The present studies were conducted, to investigate the effect of HDL and other plasma lipoproteins on prostaglandin synthesis by the Langendorff-perfused rabbit heart preparation. We report that HDL stimulates cardiac PGIp synthesis, and that this stimulation is at least partly due to the activation of a cardiac phospholipase that increases the amount of endogenous arachidonic acid available for PGIp synthesis
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