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Am J Physiol Heart Circ Physiol 283: H461-H467, 2002; doi:10.1152/ajpheart.00701.2001
0363-6135/02 $5.00
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Vol. 283, Issue 2, H461-H467, August 2002

TRANSLATIONAL PHYSIOLOGY
Lipopolysaccharide induces apoptosis in adult rat ventricular myocytes via cardiac AT1 receptors

Hai Ling Li*, Jun Suzuki*, Evelyn Bayna, Fu-Min Zhang, Erminia Dalle Molle, Aaron Clark, Robert L. Engler, and Wilbur Y. W. Lew

Cardiology Section, Department of Medicine, Veterans Affairs, San Diego Healthcare System, and University of California, San Diego, San Diego, California 92161

Lipopolysaccharide (LPS) from gram-negative bacteria circulates in acute, subacute, and chronic conditions. It was hypothesized that LPS directly induces cardiac apoptosis. In adult rat ventricular myocytes (isolated with depyrogenated digestive enzymes to minimize tolerance), LPS (10 ng/ml) decreased the ratio of Bcl-2 to Bax at 12 h; increased caspase-3 activity at 16 h; and increased annexin V, propidium iodide, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining at 24 h. Apoptosis was blocked by the caspase inhibitor benzyloxycarbonyl-valine-alanine-aspartate fluoromethylketone (Z-VAD-fmk), captopril, and angiotensin II type 1 receptor (AT1) inhibitor (losartan), but not by inhibitors of AT2 receptors (PD-123319), tumor necrosis factor-alpha (TNFRII:Fc), or nitric oxide (NG-monomethyl-L-arginine). Angiotensin II (100 nmol/l) induced apoptosis similar to LPS without additive effects. LPS in vivo (1 mg/kg iv) increased apoptosis in left ventricular myocytes for 1-3 days, which dissipated after 1-2 wk. Losartan (23 mg · kg-1 · day-1 in drinking water for 3 days) blocked LPS-induced in vivo apoptosis. In conclusion, low levels of LPS induce cardiac apoptosis in vitro and in vivo by activating AT1 receptors in myocytes.

endotoxemia; programmed cell death; cardiac renin-angiotensin; angiotensin II

* H. L. Li and J. Suzuki contributed equally to this work.




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