Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue. / Olsen, Kristine B; Braunstein, Thomas H; Sørensen, Charlotte M; Axelsen, Lene Nygaard; Holstein-Rathlou, Niels-Henrik; Nielsen, Morten S.

I: Scandinavian Journal of Clinical and Laboratory Investigation. Supplement, Bind 71, Nr. 6, 06.07.2011, s. 492.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Olsen, KB, Braunstein, TH, Sørensen, CM, Axelsen, LN, Holstein-Rathlou, N-H & Nielsen, MS 2011, 'Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue', Scandinavian Journal of Clinical and Laboratory Investigation. Supplement, bind 71, nr. 6, s. 492. https://doi.org/10.3109/00365513.2011.589009

APA

Olsen, K. B., Braunstein, T. H., Sørensen, C. M., Axelsen, L. N., Holstein-Rathlou, N-H., & Nielsen, M. S. (2011). Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue. Scandinavian Journal of Clinical and Laboratory Investigation. Supplement, 71(6), 492. https://doi.org/10.3109/00365513.2011.589009

Vancouver

Olsen KB, Braunstein TH, Sørensen CM, Axelsen LN, Holstein-Rathlou N-H, Nielsen MS. Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue. Scandinavian Journal of Clinical and Laboratory Investigation. Supplement. 2011 jul 6;71(6):492. https://doi.org/10.3109/00365513.2011.589009

Author

Olsen, Kristine B ; Braunstein, Thomas H ; Sørensen, Charlotte M ; Axelsen, Lene Nygaard ; Holstein-Rathlou, Niels-Henrik ; Nielsen, Morten S. / Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue. I: Scandinavian Journal of Clinical and Laboratory Investigation. Supplement. 2011 ; Bind 71, Nr. 6. s. 492.

Bibtex

@article{ca5bf848da4043dfa9c019715ae6fd1e,
title = "Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue",
abstract = "Abstract Aim. Atrial angiotensin II (Ang II) levels are increased in atrial fibrillation and are believed to be important in the pathogenesis of atrial arrhythmias. Ang II reduces intercellular coupling by inhibiting gap junctions (connexins) and may thereby increase the risk of reentry arrhythmia. The aim of the current study was to investigate the acute effect of Ang II on conduction velocity (CV) in atrial tissue from normal and chronically infarcted rats. Methods. Contractile force was measured and CV was determined from the conduction time between electrodes placed on the tissue preparation. Expression of AT1a and AT1b receptors was examined by real-time PCR. Results. Acute stimulation with Ang II did not affect CV in tissue from auricle or atrial free wall. A transient 6.5 ± 3.6{\%} increase in resting tension was observed in atrial free wall preparations, indicating that receptors are present and functional in the free wall preparation. The difference between free wall and auricle was probably not caused by differences in receptor expression since equal amounts of AT1 mRNA were present. To test if myocardial infarction (MI) sensitizes the atrium to Ang II, free atrial wall from rats subjected to 4-5 weeks ventricular MI was examined. Although CV was significantly reduced by MI, no effect on CV of Ang II was seen. Conclusion. Ang II does not acutely regulate CV in tissue preparations from the free wall of the left atria or the left auricle. Although ventricular MI reduces CV, this does not sensitize the atria to Ang II.",
keywords = "Faculty of Health and Medical Sciences",
author = "Olsen, {Kristine B} and Braunstein, {Thomas H} and S{\o}rensen, {Charlotte M} and Axelsen, {Lene Nygaard} and Niels-Henrik Holstein-Rathlou and Nielsen, {Morten S}",
year = "2011",
month = "7",
day = "6",
doi = "10.3109/00365513.2011.589009",
language = "English",
volume = "71",
pages = "492",
journal = "Scandinavian Journal of Clinical and Laboratory Investigation. Supplement",
issn = "0085-591X",
publisher = "Taylor & Francis",
number = "6",

}

RIS

TY - JOUR

T1 - Angiotensin II does not acutely regulate conduction velocity in rat atrial tissue

AU - Olsen, Kristine B

AU - Braunstein, Thomas H

AU - Sørensen, Charlotte M

AU - Axelsen, Lene Nygaard

AU - Holstein-Rathlou, Niels-Henrik

AU - Nielsen, Morten S

PY - 2011/7/6

Y1 - 2011/7/6

N2 - Abstract Aim. Atrial angiotensin II (Ang II) levels are increased in atrial fibrillation and are believed to be important in the pathogenesis of atrial arrhythmias. Ang II reduces intercellular coupling by inhibiting gap junctions (connexins) and may thereby increase the risk of reentry arrhythmia. The aim of the current study was to investigate the acute effect of Ang II on conduction velocity (CV) in atrial tissue from normal and chronically infarcted rats. Methods. Contractile force was measured and CV was determined from the conduction time between electrodes placed on the tissue preparation. Expression of AT1a and AT1b receptors was examined by real-time PCR. Results. Acute stimulation with Ang II did not affect CV in tissue from auricle or atrial free wall. A transient 6.5 ± 3.6% increase in resting tension was observed in atrial free wall preparations, indicating that receptors are present and functional in the free wall preparation. The difference between free wall and auricle was probably not caused by differences in receptor expression since equal amounts of AT1 mRNA were present. To test if myocardial infarction (MI) sensitizes the atrium to Ang II, free atrial wall from rats subjected to 4-5 weeks ventricular MI was examined. Although CV was significantly reduced by MI, no effect on CV of Ang II was seen. Conclusion. Ang II does not acutely regulate CV in tissue preparations from the free wall of the left atria or the left auricle. Although ventricular MI reduces CV, this does not sensitize the atria to Ang II.

AB - Abstract Aim. Atrial angiotensin II (Ang II) levels are increased in atrial fibrillation and are believed to be important in the pathogenesis of atrial arrhythmias. Ang II reduces intercellular coupling by inhibiting gap junctions (connexins) and may thereby increase the risk of reentry arrhythmia. The aim of the current study was to investigate the acute effect of Ang II on conduction velocity (CV) in atrial tissue from normal and chronically infarcted rats. Methods. Contractile force was measured and CV was determined from the conduction time between electrodes placed on the tissue preparation. Expression of AT1a and AT1b receptors was examined by real-time PCR. Results. Acute stimulation with Ang II did not affect CV in tissue from auricle or atrial free wall. A transient 6.5 ± 3.6% increase in resting tension was observed in atrial free wall preparations, indicating that receptors are present and functional in the free wall preparation. The difference between free wall and auricle was probably not caused by differences in receptor expression since equal amounts of AT1 mRNA were present. To test if myocardial infarction (MI) sensitizes the atrium to Ang II, free atrial wall from rats subjected to 4-5 weeks ventricular MI was examined. Although CV was significantly reduced by MI, no effect on CV of Ang II was seen. Conclusion. Ang II does not acutely regulate CV in tissue preparations from the free wall of the left atria or the left auricle. Although ventricular MI reduces CV, this does not sensitize the atria to Ang II.

KW - Faculty of Health and Medical Sciences

U2 - 10.3109/00365513.2011.589009

DO - 10.3109/00365513.2011.589009

M3 - Journal article

VL - 71

SP - 492

JO - Scandinavian Journal of Clinical and Laboratory Investigation. Supplement

JF - Scandinavian Journal of Clinical and Laboratory Investigation. Supplement

SN - 0085-591X

IS - 6

ER -

ID: 33746070