Prostacyclin receptor/thromboxane receptor interactions and cellular responses in human atherothrombotic disease

Gleim, Scott; Kasza, Zsolt; Martin, Kathleen A.; Hwa, John

doi:10.1007/s11883-009-0035-5

Cited by 20 publications

(20 citation statements)

References 63 publications

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“…57 Given that NO and PGI 2 are reduced in preeclampsia, it is reasonable to suggest that negative regulation of TP is also impaired. Animal studies have confirmed this hypothesis.…”

Section: Hypertensionmentioning

confidence: 99%

Maternal Vascular Physiology in Preeclampsia

Goulopoulou

2017

Hypertension

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“…57 Given that NO and PGI 2 are reduced in preeclampsia, it is reasonable to suggest that negative regulation of TP is also impaired. Animal studies have confirmed this hypothesis.…”

Section: Hypertensionmentioning

confidence: 99%

Maternal Vascular Physiology in Preeclampsia

Goulopoulou

2017

Hypertension

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“…Furthermore, PGI 2 also stimulates the release of EDRF [28]. In addition, NO which accounts for the actions of EDRF [29], potentiates anti-aggregatory properties of PGI 2 ; they both can prevent platelet aggregation together at concentrations which on their own too low to inhibit aggregation [30,31]. NO also inhibits platelet adhesion to the vascular endothelium which contributes to nonthrombogenicity of endothelial cell [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Adaptação de um sistema de ensaio biológico para detecção de fatores relaxantes endoteliais derivados do endocárdio atrial canino

Chua¹,

Évora²,

Celotto³

et al. 2009

Rev Bras Cir Cardiovasc

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Adaptação de um sistema de ensaio biológico para detecção de fatores relaxantes endoteliais derivados do endocárdio atrial caninoAdaptation of bioassay to detect endotheliumderived relaxing factors from the canine atrial endocardium Abstract Objective: The aim of this study was to assess the release of endothelium-derived relaxing factors from the endocardium of canine atrial appendage.Method: To study the release of endothelium-derived relaxing factor (EDRF) from intact atrial endocardial endothelium, tube-shaped sutures of canine atrial appendages were performed and effluents from these tubes were bioassayed (isolated perfused organ chamber system) for detection of EDRF in canine coronary artery.Results: Effluent from the right atrial appendage caused a relaxation of 58.4 + 10.1% and the left atrial appendage 74.9 + 8.5% from the initial prostagladin FF2α α α α α contraction in coronary artery. No significant statistical difference was detected in effluent from the right and left atrial appendages. This relaxation was abolished by treating the heart tubes with Triton X-100 and reduced by treatment with LNMMA, a competitive inhibitor of nitric oxide and with indomethacin, an inhibitor of the cyclo-oxygenase pathway, also indicating the release of vasodilatory prostanoids from the endocardial endothelium.Conclusion: This study showed for the first time, in vitro luminal release of EDRF and prostacyclin from the canine heart atrium. The ability of the endocardial endothelium to produce these factors could play an important role in preventing thrombus formation in the cardiac chambers. 226CHUA, YL ET AL -Adaptation of bioassay to detect endotheliumderived relaxing factors from the canine atrial endocardium Bras Cir Cardiovasc 2009; 24(2): 225-232 regulation of receptors when the cells are cultured and the response of the cultured endothelium to agonists can be altered [13,14]. In the present experiments, a bioassay technique was developed to detect luminal release of endothelium-derived relaxing factors from intact canine atrial endocardium. Rev METHODS Bioassay techniqueHeartworm free mongrel dogs (25-30 kg; n=10) of either sex were anesthetized with intravenous pentobarbital sodium (30 mg/kg bolus injection; Fort Dodge Laboratories) and exsanguinated via the carotid arteries; the beating heart was excised and immersed in cool, oxygenated physiological salt solution of the following millimolar composition: NaCl, 118.3; KCl, 4.7; MgSO 4 , 1.2; KH 2 PO 4 , 1.22; CaCl 2 , 2.5; NaHCO 3 , 25.0 and glucose, 11.1 (control solution). The procedures and the handling of the animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Mayo Foundation.The left circumflex coronary artery was carefully dissected free from the heart and placed in control solution. A coronary ring of about 3 mm was cut and the endothelium removed with a pair of watchmakers forceps. This procedure effectively removes endothelium from the coronary ring without affecting the smooth muscle ability to contract or r...

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“…6 Because of this contradictory action of PGI2 and TXA2, many aspects of cardiovascular disease have been explained by alterations in the balance between PGI2 and TXA2 during the interactions between platelets and the vessel wall (Figure 1). 28,29 Lessons From Clinical Experience With COX-2 Selective Inhibitors…”

Section: Kawabe J Et Almentioning

confidence: 99%

Prostacyclin in Vascular Diseases - Recent Insights and Future Perspectives -

Kawabe

Ushikubi

Hasebe

2010

Circ J

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Prostacyclin (PGI2) is one of the important vascular prostanoids, the effects of which counteract those of thromboxane (TXA2), and these 2 prostanoids provide an important balance in cardiovascular homeostasis. The clinical experience of COX-2 selective inhibitors having unexpected adverse effects in patients with cardiovascular risk has opened up a debate about the role of COX-2-derived prostanoids in vascular pathophysiology. PGI2 is a major anti-atherogenic prostanoid produced by COX-2 in vascular cells, including endothelial and vascular smooth muscle cells. The balance between COX-2-derived PGI2, COX-1-derived TXA2, and other COX-2-mediated atherogenic prostanoids is a crucial factor in determining pathophysiological outcomes. Recent studies using stable PGI2 analogs and genetically deficient mice have revealed novel effects of PGI2 on its target cells, such as endothelial and endothelial progenitor cells. The role PGI2 in the physiology and pathophysiology of vascular diseases is reviewed and the recent findings linking PGI2, COX-2 and atherothrombosis are summarized. (Circ J 2010; 74: 836 - 843)

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Prostacyclin receptor/thromboxane receptor interactions and cellular responses in human atherothrombotic disease

Cited by 20 publications

References 63 publications

Maternal Vascular Physiology in Preeclampsia

Maternal Vascular Physiology in Preeclampsia

Adaptação de um sistema de ensaio biológico para detecção de fatores relaxantes endoteliais derivados do endocárdio atrial canino

Prostacyclin in Vascular Diseases - Recent Insights and Future Perspectives -

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