1989Journal of Cardiovascular PharmacologyRequires access

Interaction Between NO Donors and Iloprost in Human Vascular Smooth Muscle, Platelets, and Leukocytes

Ryszard J. Gryglewski, Ryszard Korbut, Elżbieta Trabka-Janik, Artur Zembowicz, M. Trybulec

Open publisher page 15 citations

Abstract

Endothelium-derived relaxing factor (EDRF) and donors of nitric oxide (NO) (glyceryl trinitrate, SIN-1--a metabolite of molsidomine--S-nitroso-N-acetyl-penicillamine, and sodium nitroprusside) but not prostacyclin and its analog, iloprost, relax strips of rabbit aorta. Strips of human coronary artery also relax when exposed to NO donors and prostacyclin; in this artery, SIN-1 and iloprost exert additive but not synergistic relaxant action. In mildly activated human platelets and leukocytes, SIN-1 and iloprost have a synergistic suppressive action. A similar synergistic thrombolytic effect between NO and prostacyclin was observed in whole rabbit blood in interactions with rabbit aortic endothelium. These findings suggest that because of this cell-selective synergism between NO donors and prostacyclin analogs, the concomitant use of molsidomine and iloprost for the treatment of ischemic heart and peripheral vascular disease should be attempted.

About this research paper

What this paper is about

Endothelium-derived relaxing factor (EDRF) and donors of nitric oxide (NO) (glyceryl trinitrate, SIN-1--a metabolite of molsidomine--S-nitroso-N-acetyl-penicillamine, and sodium nitroprusside) but not prostacyclin and its analog, iloprost, relax strips of rabbit aorta. Strips of human coronary artery also relax when exposed to NO donors and prostacyclin; in this artery, SIN-1 and iloprost exert additive but not synergistic relaxant action. In mildly activated human platelets and leukocytes, SIN-1 and iloprost have a synergistic suppressive action. A similar synergistic thrombolytic effect between NO and prostacyclin was observed in whole rabbit blood in interactions with rabbit aortic endothelium. These findings suggest that because of this cell-selective synergism between NO donors and prostacyclin analogs, the concomitant use of molsidomine and iloprost for the treatment of ischemic heart and peripheral vascular disease should be attempted.

Why it matters

OpenAlex reports 15 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Endothelium-derived relaxing factor (EDRF) and donors of nitric oxide (NO) (glyceryl trinitrate, SIN-1--a metabolite of molsidomine--S-nitroso-N-acetyl-penicillamine, and sodium nitroprusside) but not prostacyclin and its analog, iloprost, relax strips of rabbit aorta. Strips of human coronary artery also relax when exposed to NO donors and prostacyclin; in this artery, SIN-1 and iloprost exert additive but not synergistic relaxant action. In mildly activated human platelets and leukocytes, SIN-1 and iloprost have a synergistic suppressive action. A similar synergistic thrombolytic effect between NO and prostacyclin was observed in whole rabbit blood in interactions with rabbit aortic endothelium. These findings suggest that because of this cell-selective synergism between NO donors and prostacyclin analogs, the concomitant use of molsidomine and iloprost for the treatment of ischemic heart and peripheral vascular disease should be attempted.

Key concepts: Iloprost, Platelet, Vascular smooth muscle, Medicine, Smooth muscle, Internal medicine, Pharmacology, Cardiology

Related papers

Back to paper searchBrowse research topicsOriginal source
Interaction Between NO Donors and Iloprost in Human Vascular Smooth Muscle, Platelets, and Leukocytes — Research Paper | ScholarLens