E icosanoids, particularly prostacyclin (PGI2) and thromboxane A2 (TxA2), have been implicated in the regulation of vascular homeostasis from the point of view of platelet-vessel wall interactions and in the regulation of blood vessel tone and hemostasis (for reviews, see references 1 and 2). However, subsequent investigations have revealed that PGI2 and other eicosanoids may also have an important role in the regulation of arterial smooth muscle cell phenotype and cellular cholesterol metabolism. The purpose of this review is to summarize recent findings on the role of eicosanoids in the regulation of smooth muscle cell proliferative capacity and cellular cholesterol content under normal physiological conditions and in an "atherogenic" environment.

https://www.ahajournals.org/doi/pdf/10.1161/01.ATV.9.4.413

Eicosanoids in regulation of arterial smooth muscle cell phenotype, proliferative capacity, and cholesterol metabolism.

Changes in antioxidant enzymes activities, aggregability and malonyldialdehyde concentration in blood platelets from patients with coronary heart disease

Recent studies indicate that short-term cholesterol feeding causes vascular hyperreactivity and/or increased tone in certain vascular beds. The present study in rats examined the effect of 3 wk of cholesterol-supplemented diet (CSD) on renal hemodynamics. We tested the hypothesis that LDL oxidized in vivo is causally related to increased renal vascular tone by adding the antioxidant drug probucol to the CSD (CSD + P). Micropuncture of surface nephrons in the CSD rats demonstrated that single nephron glomerular filtration rate (SNGFR) and single nephron afferent plasma flow (QA) were markedly lower than in normal rats, whereas glomerular capillary pressure (PGC), afferent arteriolar resistance (RA), and single nephron filtration fraction (SNFF) were higher. In the CSD + P animals, almost all of these hemodynamic abnormalities were absent. TXB2 and PGE2 were increased in proximal tubule fluid and urine in the CSD rats, but normal in the CSD + P group. Infusion of a TXA2 receptor antagonist into the suprarenal aorta of CSD rats caused a rapid return to normal of RBF (renal blood flow), GFR (glomerular filtration rate), SNGFR, QA, RA, PGC, and Kf (ultrafiltration coefficient). Our observations demonstrate that cholesterol feeding leads to renal vasoconstriction, which appears to be mediated largely by increased TXA2 production. The fact that probucol prevented the hemodynamic abnormalities as well as the increased TX production is consistent with the hypothesis that LDL oxidized in vivo initiates events leading to TX mediated vasoconstriction.

/pdf/renal-vasoconstriction-caused-by-short-term-cholesterol-46hbqkedre.pdf

Renal vasoconstriction caused by short-term cholesterol feeding is corrected by thromboxane antagonist or probucol.

Prostaglandins (PGs), thromboxanes (Txs), and leukotrienes (LTs) play a relevant role in cardiovascular physiology and pathophysiology. Recent reports concerning cardiovascular risk associated with cyclooxygenase-2 selective inhibitors have prompted questions about the "protective" or "deleterious" role of each COX isoform in cardiovascular disease, and the cloning and expression of inducible PGE-synthase (PGES) open the possibility that PGES could be a new therapeutical target in this context. Predominance of constricting or relaxing prostanoids depends not only on COX activity but also to downstream enzymes such as PGI-synthase (PGIS) and PGES. In the vessel wall, PGIS and PGES seem to be major downstream enzymes in the endothelium and smooth muscle, respectively. Like COX, activity of these enzymes can also be regulated by several factors, which include nitrogen oxides, cytokines, and lipid peroxides. LTs are important inflammatory mediators also involved in the pathophysiology of cardiovascular disease, which are targets for pharmacological intervention. Unlike COX pathway, the biosynthesis of chemotactic and vaso-constrictor LTs in the vasculature strongly depends on leukocyte recruitment and activation, and on cell-cell interaction between leukocytes and vascular cells in the inflamed areas. The present review emphasizes the role of vascular-derived prostanoids and LTs on atherosclerosis.

Cyclooxygenase and 5‐Lipoxygenase Pathways in the Vessel Wall: Role in Atherosclerosis

Under physiological conditions human blood platelets play a beneficial role in fibrinolysis and regulate the balance with prostacyclin and other factors derived from the endothelium. In response to endothelial injury, adherence of platelets to the denuded arterial surface, platelet aggregation, release of mitogens and subsequent cell proliferation characterize early fibrous plaque lesions. 'Native' atherogenic plasma lipoproteins which are abundant in hypercholesterolemia have been found to play a subtle role in the development of atherosclerosis. In addition, lipoproteins modulate platelet function and alter the susceptibility of platelets to different stimulating agents. The properties of 'modified' atherogenic lipoproteins also seem to be well documented with respect to atherogenesis. After uptake by macrophages, modified atherogenic plasma lipoproteins are thought to contribute to formation of fatty streak lesions. On the other hand, modified atherogenic lipoproteins may directly promote endothelial injury and thus favour enhanced endothelial-platelet interactions. However, the direct effects of modified atherogenic lipoproteins on platelet function have not been revealed in detail. Recent findings have documented that activated platelets themselves may promote modification of atherogenic plasma lipoproteins and thus contribute to enhanced foam cell formation. Therefore stimulation of thrombocytes, and their interaction with native and modified lipoproteins must be considered an important factor in the current concept of atherogenesis.

Platelets and the lipoproteins: native, modified and platelet modified lipoproteins.

An improved malondialdehyde assay for estimation of thromboxane synthase activity in washed human blood platelets.

Low density lipoprotein (LDL) from male volunteers stimulated the thromboxane formation by human platelets.

Inhibition of prostaglandin I2 (PGI2) formation by LDL-cholesterol or LDL-peroxides?

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An improved malondialdehyde assay for estimation of thromboxane synthase activity in washed human blood platelets.

Low density lipoprotein (LDL) from male volunteers stimulated the thromboxane formation by human platelets.

Inhibition of prostaglandin I2 (PGI2) formation by LDL-cholesterol or LDL-peroxides?