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Details

Autor(en) / Beteiligte
Titel
Myocardial infarction does not change Angiotensin II sensitivity of rat atria
Ist Teil von
  • The FASEB journal, 2006-03, Vol.20 (5), p.LB12-LB12
Ort / Verlag
Federation of American Societies for Experimental Biology
Erscheinungsjahr
2006
Link zum Volltext
Quelle
Wiley-Blackwell Full Collection
Beschreibungen/Notizen
  • Treatment with drugs inhibiting Angiotensin II (Ang II) formation has been successfully used to reduce the risk of atrial fibrillation after myocardial infarction. The aim of this study was to investigate whether myocardial infarction affects the sensitivity of atrial tissue to Ang II. We examined the effect of Ang II on conduction velocity (CV) and contractility in tissue strips from isolated left atria and left auricles from rats. The tissue strips were mounted in a myograph and superfused with oxygenated buffer. CV was determined from the conduction time between electrodes placed on the longitudinal axis of the tissue strip. Ang II was added to the superfusate at three different concentrations (1 μM, 100 nM and 10 nM) in separate experiments. The results show that Ang II has no effect on atrial CV in control rats at any dose tested (n=6). In rats subjected to 4–5 weeks of MI, CV was likewise unaffected by stimulation with Ang II (1 μM, n=13), but CV was significantly slower than in the control group. Furthermore, Ang II does not affect the active force during contraction under any condition tested. However, Ang II increased the resting tension in tissue from the free atrial wall in both control and infarcted animals. This effect was not seen in tissue from the left auricle. This indicates that there are differences in the Ang II receptor population in the auricle and the free wall from the left atria. In conclusion myocardial infarction does not change the Ang II sensitivity of rat atria. Ang II only affected resting tension and this effect was only observed in the free wall and not in the auricle.
Sprache
Englisch
Identifikatoren
ISSN: 0892-6638
eISSN: 1530-6860
DOI: 10.1096/fasebj.20.5.LB12-c
Titel-ID: cdi_crossref_primary_10_1096_fasebj_20_5_LB12_c
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