AT(2) receptor-mediated vasodilation in the heart: effect of myocardial infarction

Citation
Mp. Schuijt et al., AT(2) receptor-mediated vasodilation in the heart: effect of myocardial infarction, AM J P-HEAR, 281(6), 2001, pp. H2590-H2596
Citations number
46
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
281
Issue
6
Year of publication
2001
Pages
H2590 - H2596
Database
ISI
SICI code
0363-6135(200112)281:6<H2590:ARVITH>2.0.ZU;2-U
Abstract
To investigate the functional consequences of postinfarct cardiac angiotens in (ANG) type 2 (AT(2)) receptor upregulation, rats underwent coronary arte ry ligation or sham operation and were infused with ANG II 3-4 wk later, wh en scar formation is complete. ANG II increased mean arterial pressure (MAP ) more modestly in infarcted animals than in sham animals. The AT(1) recept or antagonist irbesartan, but not the AT(2) receptor antagonist PD123319, d ecreased MAP and antagonized the ANG II-mediated systemic hemodynamic effec ts. Myocardial (MVC) but not renal vascular conductance (RVC) was diminishe d in infarcted versus sham rats. ANG II did not affect MVC and reduced RVC in all rats. MVC was unaffected by irbesartan and PD123319 in all animals. However, with PD123319, ANG II reduced MVC in sham but not infarcted animal s, and, with irbesartan, ANG II increased MVC in infarcted but not sham ani mals. Irbesartan increased RVC and antagonized the ANG II-mediated renal ef fects in all animals. RVC, at baseline or with ANG II, was not affected by PD123319 in infarcted and sham animals. In conclusion, coronary but not ren al AT(2) receptor stimulation results in vasodilation, and this effect is e nhanced in infarcted rats.