English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Abstract —To examine the relevance of angiotensin II type 1 receptor (AT1 R) expression in the determination of myocardial function after ischemia/reperfusion, Sprague-Dawley rats were treated intravenously with antisense oligodeoxynucleotides (AS-ODNs) directed at AT1 R mRNA (100 μg/rat, n=9) or scrambled antisense oligodeoxynucleotides (Scr-ODNs, 100 μg/rat, n=6). Both AS-ODNs and Scr-ODNs were given along with 300 μg/rat of liposome DOTAP/DOPE, a positive electron carrier (wt:wt=1:1). The hearts from AS-ODN– or Scr-ODN–treated rats were excised 24 hours later, perfused in vitro, and subjected to 25 minutes of global ischemia followed by 30 minutes of reperfusion. Parallel groups of rats were given the specific AT1 R antagonist losartan (10 mg/kg IV, n=6) or saline (n=7) 4 to 6 hours before excising the hearts. Ischemia/reperfusion resulted in a significant increase in myocardial AT1 R expression (autoradiography and binding assay) and myocardial dysfunction, indicated by increases in coronary perfusion pressure and left ventricular end-diastolic pressure and a decrease in developed left ventricular pressure (allP &lt;0.01 versus baseline) in the saline-treated group. AT1 R protein and mRNA levels also increased in ischemic/reperfused myocardial tissues. Administration of AS-ODNs or losartan, but not Scr-ODNs, preserved myocardial function and blocked the increased AT1 R binding after ischemia/reperfusion (bothP &lt;0.01). Myocardial AT1 R mRNA levels were not affected by either AS-ODNs or losartan, and the AT1 R protein levels were significantly reduced by AS-ODN, but not losartan, treatment. Plasma angiotensin II levels increased after administration of losartan but not after administration of AS-ODNs. These observations imply a critical role of AT1 R upregulation in determining myocardial function immediately after ischemia/reperfusion. AS-ODNs to AT1 R mRNA may be more beneficial than losartan, because losartan does not affect the plasma angiotensin II level. The sustained increase in AT1 R mRNA, but diminished protein expression, in rat hearts treated with AS-ODNs suggests that AS-ODNs block AT1 R at the translational level.

Critical Role of AT 1 Receptor Expression After Ischemia/Reperfusion in Isolated Rat Hearts

Critical Role of AT ₁ Receptor Expression After Ischemia/Reperfusion in Isolated Rat Hearts