Limits...
Short-term effect of the HMG-CoA reductase inhibitor rosuvastatin on erythrocyte nitric oxide synthase activity.

Ludolph B, Bloch W, Kelm M, Schulz R, Kleinbongard P - Vasc Health Risk Manag (2007)

Bottom Line: Afterwards RBC-NOS activity and RBC deformability were determined.The NOS inhibitor NG- monomethyl-L-arginine reversed the stimulatory effect of rosuvastatin on RBC-NOS activity.This NO dependent effect of rosuvastatin might have an important influence on microcirculation and may offer new perspectives for the therapeutic use of statins.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Medical Clinic I, University Hospital RTWH Aachen, Germany.

ABSTRACT
Prevention and treatment of cardiovascular disorders by HMG-CoA reductase inhibitors (or statins), beyond their lipid-lowering properties, have been demonstrated including activation of the endothelial nitric oxide synthase (eNOS). Beside endothelial cells, red blood cells (RBCs) possess NOS and produce nitric oxide (NO), which contributes to RBC deformability. The present study tested the capacity of statins to activate NOS in RBCs and subsequently to modulate RBC deformability in vitro. Blood samples of healthy young volunteers were incubated with or without rosuvastatin. Afterwards RBC-NOS activity and RBC deformability were determined. Rosuvastatin incubation significantly increased NOS phosphorylation, NOS dependent NO-formation, and RBC deformability. The NOS inhibitor NG- monomethyl-L-arginine reversed the stimulatory effect of rosuvastatin on RBC-NOS activity. This NO dependent effect of rosuvastatin might have an important influence on microcirculation and may offer new perspectives for the therapeutic use of statins.

Show MeSH

Related in: MedlinePlus

Effect of rosuvastatin on RBC-NOS activity and RBC deformability. Parallel to the RBC-NOS activity (detected as accumulated plasma nitrite concentration) flow rate of RBC through a microfilter (as a measure of RBC deformability) were determined after incubation of whole blood with (black squares) and without rosuvastatin (white squares).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2350149&req=5

fig2: Effect of rosuvastatin on RBC-NOS activity and RBC deformability. Parallel to the RBC-NOS activity (detected as accumulated plasma nitrite concentration) flow rate of RBC through a microfilter (as a measure of RBC deformability) were determined after incubation of whole blood with (black squares) and without rosuvastatin (white squares).

Mentions: RBC deformability increased significantly after incubation with rosuvastatin from 1.96 ± 0.34 ml/min (controls) to 2.63 ± 0.31 ml/min (p < 0.036). Plasma nitrite levels correlated to RBC deformability (R = 0.59, p < 0.0001; Figure 2).


Short-term effect of the HMG-CoA reductase inhibitor rosuvastatin on erythrocyte nitric oxide synthase activity.

Ludolph B, Bloch W, Kelm M, Schulz R, Kleinbongard P - Vasc Health Risk Manag (2007)

Effect of rosuvastatin on RBC-NOS activity and RBC deformability. Parallel to the RBC-NOS activity (detected as accumulated plasma nitrite concentration) flow rate of RBC through a microfilter (as a measure of RBC deformability) were determined after incubation of whole blood with (black squares) and without rosuvastatin (white squares).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2350149&req=5

fig2: Effect of rosuvastatin on RBC-NOS activity and RBC deformability. Parallel to the RBC-NOS activity (detected as accumulated plasma nitrite concentration) flow rate of RBC through a microfilter (as a measure of RBC deformability) were determined after incubation of whole blood with (black squares) and without rosuvastatin (white squares).
Mentions: RBC deformability increased significantly after incubation with rosuvastatin from 1.96 ± 0.34 ml/min (controls) to 2.63 ± 0.31 ml/min (p < 0.036). Plasma nitrite levels correlated to RBC deformability (R = 0.59, p < 0.0001; Figure 2).

Bottom Line: Afterwards RBC-NOS activity and RBC deformability were determined.The NOS inhibitor NG- monomethyl-L-arginine reversed the stimulatory effect of rosuvastatin on RBC-NOS activity.This NO dependent effect of rosuvastatin might have an important influence on microcirculation and may offer new perspectives for the therapeutic use of statins.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Medical Clinic I, University Hospital RTWH Aachen, Germany.

ABSTRACT
Prevention and treatment of cardiovascular disorders by HMG-CoA reductase inhibitors (or statins), beyond their lipid-lowering properties, have been demonstrated including activation of the endothelial nitric oxide synthase (eNOS). Beside endothelial cells, red blood cells (RBCs) possess NOS and produce nitric oxide (NO), which contributes to RBC deformability. The present study tested the capacity of statins to activate NOS in RBCs and subsequently to modulate RBC deformability in vitro. Blood samples of healthy young volunteers were incubated with or without rosuvastatin. Afterwards RBC-NOS activity and RBC deformability were determined. Rosuvastatin incubation significantly increased NOS phosphorylation, NOS dependent NO-formation, and RBC deformability. The NOS inhibitor NG- monomethyl-L-arginine reversed the stimulatory effect of rosuvastatin on RBC-NOS activity. This NO dependent effect of rosuvastatin might have an important influence on microcirculation and may offer new perspectives for the therapeutic use of statins.

Show MeSH
Related in: MedlinePlus