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Angiotensin II in the presence of an AT1 receptor blockade potentiates the coronary vasodilation mediated by bradykinin in the isolated rat heart
Author(s) -
Fan Jingsong,
Hu Lufei,
Zimmitti Clare,
Matera Damian,
Weldon Steven,
Kerr Steve,
Seidler Randolph,
Madwed Jeff
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1111-a
Subject(s) - telmisartan , bradykinin , angiotensin ii , medicine , vasodilation , endocrinology , angiotensin ii receptor type 1 , stimulation , endothelial dysfunction , angiotensin receptor , blockade , receptor , renin–angiotensin system , blood pressure
Our aim of this study was to explore the effect of Angiotensin II (Ang II) induced hypertension on coronary endothelial function in the presence of Ang II receptor blockade. Methods SD rats were continuously infused with Ang II (300 ng/kg/min, s.c.) via ALZET minipump for 14 days. Vehicle or telmisartan (10 mg/kg/day) was administered orally once daily. On day 14, coronary flow rate (CFR) in response to bradykinin (BK, 0.1 to 100 nM) was measured in a Langendorff‐perfused isolated heart preparation. Results Mean arterial pressure (MAP) increased from 97±3 mmHg (day0) to 159±9 mmHg (day14) in the vehicle + Ang II group. Telmisartan prevented the Ang II‐induced increase in MAP. CFR induced by BK was significantly reduced in the vehicle+Ang II group compared to that in normotensive rats, indicating an impaired endothelial response in the coronary arteries. In contrast, CFR changes to BK in the telmisartan‐treated group were significantly higher than that in normotensive group, indicating an improvement in coronary endothelial function. Conclusion Ang II impaired coronary endothelial function, but in the presence of telmisartan improved coronary endothelial function above that of normotensive controls. The potentiation effect seen in telmisartan group most likely involves the actions of AII on AT2 receptors stimulation. *JF and LH contributed equally