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Trends in Comparative Biochemistry & Physiology   Volumes    Volume 8 
Differential location of angiotensin II receptor subtypes and potential effects of their antagonists on cardioprotection in a rat heart model
Anwar B. Bikhazi, Khalil M. Bitar, Nuhad E. Abou Zeid, Wael A. Jaroudi
Pages: 91 - 97
Number of pages: 7
Trends in Comparative Biochemistry & Physiology
Volume 8 

Copyright © 2001 Research Trends. All rights reserved


This study/review is aimed at assessing the binding constants and consequently the effective role of Angiotensin II (Ang II) on endothelial and cardiac myocytes in the presence and absence of Angiotensin II type 1 receptor (AT1-R) and Angiotensin II type 2 receptor (AT2-R) antagonists in perfused healthy Sprague-Dawley rat hearts. A heart perfusion method was used, the inlet via the aortic lumen, and the outlet via the right atrium and the measured concentration of Ang II in the effluent with time is plotted using concurrently a physical model describing a 1:1 ligand-receptor binding stoichiometry at the microvascular endothelium, and after CHAPS-treatment with cardiac myocytes. A first order impulse function allowed the calculation of the forward binding constant (kn), the reversible constant (k-n), the dissociation constant (kd), and the residency time constant (τ) from the curve fittings. The AT1-R antagonists [Losartan (LO) and Irbesartan (IR)], and the AT2-R antagonist [PD 123319(PD)] were dissolved in perfusate at 2μg/mL concentrations. Results show that the AT1-R embedded at endothelial versus myocyte sites did not show identical affinities. The presence of LO compared to IR in perfusate showed increase in binding affinity of Ang II with the AT2-R at the endothelial as well as at the cardiac myocyte sites. PD effectively reduced the binding affinity of Ang II with the AT1-R at the endothelial site, however induced better affinity at the cardiac myocyte site. In conclusion, LO and IR showed differences in pharmacodynamics. In addition, the AT1-R and AT2-R are differentially located at the endothelial versus the cardiac myocyte sites, and AT2-R antagonist may preferentially mediate inhibition of cell proliferation and angiogenesis, and consequently induce cardioprotective effects at the coronary endothelial site.

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