Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/17524
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Rajendran, S. | - |
dc.contributor.author | Chirkov, Y. | - |
dc.contributor.author | Campbell, D. | - |
dc.contributor.author | Horowitz, J. | - |
dc.date.issued | 2005 | - |
dc.identifier.citation | Journal of Cardiovascular Pharmacology, 2005; 46(4):459-463 | - |
dc.identifier.issn | 0160-2446 | - |
dc.identifier.issn | 1533-4023 | - |
dc.identifier.uri | http://hdl.handle.net/2440/17524 | - |
dc.description.abstract | Patients with ischemic heart disease have platelets that are resistant to the anti-aggregatory effects of nitric oxide (NO) donors. This NO resistance is associated with increased whole blood superoxide radical (O2−) content. Angiotensin II (Ang II) has been shown to augment O2− formation. Recent studies have demonstrated that angiotensin-(1-7) [Ang-(1-7)] has opposite actions to those of Ang II in the vasculature. This study compares the effects of Ang-(1-7) and Ang II on platelet aggregation and platelet responsiveness to the NO donor sodium nitroprusside (SNP). Platelet aggregation was induced by the thromboxane A2 mimetic U46619 (1-5 μmol/L), and the inhibitory effects of SNP (10 μmol/L) on the rate and extent of aggregation were quantified. Ang II did not induce aggregation, but 10-100 nmol/L Ang II potentiated U46619-induced aggregation by 21 ± 6% in the absence and by 26 ± 9% in the presence of SNP (P < 0.01 for both), in blood samples from 8 normal subjects. By contrast, Ang-(1-7) alone did not affect platelet aggregation, but 10-100 nmol/L Ang-(1-7) potentiated the anti-aggregatory effects of SNP in blood samples from both normal subjects (n = 17) and patients with acute coronary syndromes (n = 17). This effect of Ang-(1-7) was bimodal, and at higher concentrations of Ang-(1-7), potentiation was abolished. The maximum incremental effects of Ang-(1-7) on inhibition of aggregation were 25 ± 4% and 28 ± 5%, for rate and extent of aggregation respectively (P < 0.01 for both), corresponding to a 2.3-fold potentiation of the anti-aggregatory effect of SNP. Platelets from patients were resistant to the anti-aggregatory effect of SNP, but potentiation of SNP effects by Ang-(1-7) was similar for patients and normal subjects. Thus, Ang-(1-7) potentiates the anti-aggregatory effects of NO donor, and may therefore counteract platelet NO resistance that accompanies cardiovascular disease. | - |
dc.description.statementofresponsibility | Sharmalar Rajendran, Yuliy Y. Chirkov, Duncan J. Campbell, and John D. Horowitz | - |
dc.language.iso | en | - |
dc.publisher | Lippincott Williams & Wilkins | - |
dc.rights | © 2005 Lippincott Williams & Wilkins, Inc. | - |
dc.source.uri | http://journals.lww.com/cardiovascularpharm/pages/articleviewer.aspx?year=2005&issue=10000&article=00009&type=abstract | - |
dc.subject | angiotensin II | - |
dc.subject | angiotensin-(1-7) | - |
dc.subject | platelet aggregation | - |
dc.subject | U46619 | - |
dc.subject | nitric oxide | - |
dc.title | Angiotensin-(1-7) enhances anti-aggregatory effects of the nitric oxide donor sodium nitroprusside | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1097/01.fjc.0000176729.51819.a6 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Rajendran, S. [0000-0001-7949-8873] | - |
dc.identifier.orcid | Horowitz, J. [0000-0001-6883-0703] | - |
Appears in Collections: | Aurora harvest 2 Medicine publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.