[Effects of angiotensin II type 1 and type 2 receptor on apoptosis].
Apoptosis, a morphological form of programmed cell death required for control of cell populations, participates in reduced tissue volume associated with ventricular scarring. Prevention of apoptosis of excessive, damaged, or nonfunctioning cardiac or of infiltrating inflammatory cells is usually beneficial for the resolution of cardiac fibrosis. Angiotensin(Ang) II, the most important peptide that mediates the effects of the renin-angiotensin system, may play an important role in hypertension, hypertrophy, and interstitial fibrosis. Furthermore, AngII induced apoptosis of human venous endothelial cells, myocyte, and vascular smooth muscular cells by caspase cascade activation, and the both blockade of AngII type(AT)1 and AT2 receptor prevents AngII induced apoptosis, whereas selective agonistic stimulation of the AT2 receptor alone induces apoptosis. When AT1 or AT2 receptors are stimulated in vivo, apoptosis is enhanced in myocytes, myofibroblasts, and media smooth muscular cells. In the case of AT1 receptor stimulation, this may occur in cardiac myocytes secondary to ventricular hypertrophy. On the other hand, AT2 receptor stimulation induced apoptosis myofibroblasts associated with reduced interstitial fibrosis. Caspase-3 participates in the pathways of apoptosis triggered by in vivo AT1 and AT2 receptor stimulations.
Ono
Hidehiko
H
Department of Hypertension and Cardiorenal Medicine, Dokkyo University School of Medicine.
Ishimitsu
Toshihiko
T
D057911:Angiotensin Receptor Antagonists; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D051381:Rats; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000502:physiology*
D057911:Angiotensin Receptor Antagonists; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin