Roles of prostanoids in the pathogenesis of cardiovascular diseases.

Abstract

The roles of prostanoids in the pathogenesis of cardiovascular diseases and in the development of pathological conditions have been examined using mice lacking the individual, specific prostanoid receptor. Prostaglandin (PG) I2 protected the heart from ischemia-reperfusion injury in a model of acute myocardial infarction. In addition, PGI2 suppressed the development of pressure overload-induced cardiac hypertrophy. Aside from its potent vasodilatory action, PGI2 contributed critically to the development of renovascular hypertension via the activation of the renin-angiotensin-aldosterone system. Thromboxane (TX) A2 and PGF2alpha were found to be the mediators of inflammatory tachycardia under a systemic inflammatory condition induced by lipopolysaccharide. Under a septic condition leading to a vascular hypo-responsive state, TXA2 worked to maintain vascular tone by inhibiting the induction of inducible nitric oxide synthase in vascular smooth muscle cells. Mice lacking the PGE2 receptor subtype EP3 had a bleeding tendency and were resistant to thromboembolism, due to a defective activation of platelets. From these studies, the important and novel roles of prostanoids in the pathogenesis of cardiovascular diseases have been clarified.

• Authors: K Yuhki, H Kashiwagi, F Kojima, J Kawabe, F Ushikubi
• Journal: International angiology : a journal of the International Union of Angiology (Int Angiol) Vol. 29 Issue 2 Suppl Pg. 19-27 (Apr 2010) ISSN: 1827-1839 [Electronic] Italy
• PMID: 20357745 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Inflammation Mediators
• Prostaglandins
• Receptors, Prostaglandin
• Thromboxane A2
• Dinoprost
• Epoprostenol

Topics

• Animals
• Blood Platelets (metabolism)
• Cardiomegaly (metabolism, prevention & control)
• Cardiovascular Diseases (genetics, metabolism, physiopathology, prevention & control)
• Dinoprost (metabolism)
• Epoprostenol (metabolism)
• Hemodynamics
• Humans
• Hypertension, Renovascular (metabolism)
• Inflammation Mediators (metabolism)
• Mice
• Mice, Knockout
• Myocardial Reperfusion Injury (metabolism, prevention & control)
• Prostaglandins (metabolism)
• Receptors, Prostaglandin (deficiency, genetics, metabolism)
• Sepsis (metabolism)
• Signal Transduction (genetics)
• Tachycardia (metabolism)
• Thromboxane A2 (metabolism)