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Journal of Cardiovascular Pharmacology and Therapeutics
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Effect of Chronic AT1 Receptor Antagonism on Postischemic Functional Recovery and AT1/AT2 Receptor Proteins in Isolated Working Rat Hearts

Rohit Moudgil, BSc

Yi Xu, MD, PhD

Vijayan Menon, BSc

Bodh I. Jugdutt, MD, FRCPC

Division of Cardiology, Department of Medicine, and the Cardiovascular Research Group, Faculty of Medicine, University of Alberta, Edmonton, Alberta

To determine whether chronic angiotensin II (Ang II) type I receptor (ATR) antagonism improves recovery of left ventricular (LV) function after ischemia-reperfusion (IR) and increases AT,R and Ang II type 2 receptor (AT2R) protein expression in isolated working rat hearts, rats were randomized to pretreatment with either losartan (30 mg/kg/day) or UP269-6 (3 mg/kg/day), or no drug (control), for 1 week or 3 weeks before IR (50 min perfusion, 25 min ischemia, 40 min reperfusion). In vitro LV work and power and ex vivo AT,R and AT2R proteins (immunoblots) were measured. Compared to baseline perfusion, LV work and power showed variable recovery in control, losartan, and UP269-6 groups. Compared to control, losartan preserved recovery of LV work and power while UP269-6 showed less recovery after IR at both 1 week and 3 weeks. Both antagonists increased AT2R but not AT,R protein. The duration of pretreatment did not affect the expression of ATR or AT2R proteins. The results indicate that chronic AT,R blockade over 1 or 3 weeks increases AT2R (not ATIR) protein expression and may preserve but not improve postischemic functional recovery compared to controls in isolated working rat hearts.

Key Words: AT1receptor • AT2 receptor • protein • working heart • ischemia-reperfusion • function

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 6, No. 2, 183-188 (2001)
DOI: 10.1177/107424840100600210
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