title: Angiotensin II may mediate apoptosis via AT1-receptors in the rat cardiac conduction system.
abstract: BACKGROUND
  Apoptosis and angiotensin II (Ang II) have been suggested as possible causes of arrhythmias. In addition, Ang II via Ang II type I (AT(1)-) receptors, has been demonstrated to induce cardiomyocyte apoptosis. The transgenic m(Ren-2)27 (TG) rat carries the additional Ren-2 gene, the expression of which results in an increase in cardiac Ang II, thus potentially affecting the cell growth/death equilibrium. In this study we have investigated the effect of Ang II, via AT(1)-receptors, on mediating apoptosis in a cardiac conduction system (SA node and AV nodes).
  
  
  METHODS
  Heart sections from male two-day, one-week and two-week TG and Sprague-Dawley (SD) rats were stained with Masson Trichrome to localise the SA and AV nodes. The sections containing SA or AV nodes were processed for quantitation of apoptotic nuclei and AT(1)-receptors.
  
  
  RESULTS
  The number of apoptotic nuclei/mm(2) in the SA and AV nodes were found to decrease from two days to two weeks in both the TG and the SD rats, and the number of apoptotic nuclei/mm(2) in the TG groups was significantly higher than that of the SD groups for all ages (p<0.05). The number of AT(1)-receptors/mm(2) in the SA node were found to decrease with increasing age, whereas the number of AT(1)-receptors/mm(2) in the AV node was increased in both TG and SD rats and the number of AT(1)-receptors/mm(2) in the three TG groups was significantly more than that of the three SD groups (p<0.05).
  
  
  CONCLUSIONS
  As a consequence of the additional renin gene in the TG rats, which results in the alteration of the local renin-angiotensin system, the numbers of AT(1)-receptors/mm(2) and apoptotic nuclei/mm(2) are increased. The number of apoptotic nuclei/mm(2) and AT(1)-receptors/mm(2) in the SA node decrease with maturation, whereas, the number of AT(1)-receptors in the AV node increase. Thus, there may be a correlation between Ang II and apoptosis in the SA node, which does not appear to be present in the AV node.
authors.affiliation: Department of Anatomy, Prince of Songkla University, Hat-Yai 90112, Thailand. uraporn.v@psu.ac.th
authors.forename: Uraporn
authors.initials: U
authors.lastname: Vongvatcharanon
authors.forename: Surapong
authors.initials: S
authors.lastname: Vongvatcharanon
authors.forename: Nisaudah
authors.initials: N
authors.lastname: Radenahmad
authors.forename: Pornpimol
authors.initials: P
authors.lastname: Kirirat
authors.forename: Pranom
authors.initials: P
authors.lastname: Intasaro
authors.forename: Prasert
authors.initials: P
authors.lastname: Sobhon
authors.forename: Terry
authors.initials: T
authors.lastname: Parker
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D030801:Animals, Genetically Modified; D017209:Apoptosis / Q000502:physiology*; D001283:Atrioventricular Node / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D002467:Cell Nucleus / Q000378:metabolism / Q000502:physiology / Q000648:ultrastructure; D005455:Fluorescent Antibody Technique; D008297:Male; D008856:Microscopy, Fluorescence; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism / Q000502:physiology*; D012849:Sinoatrial Node / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II