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Angiotensin preconditioning of the heart: evidence for redox signaling.
Cell Biochem Biophys. 2006; 44(1):103-10.CB

Abstract

Angiotensin II (Ang II) has been found to exert preconditioning-like effect on mammalian hearts. Diverse mechanisms are known to exist to explain the cardioprotective abilities of Ang II preconditioning. The present study hypothesized, based on the recent report that Ang II generates reactive oxygen species (ROS) through NADPH oxidase, that Ang II preconditioning occurs through redox cycling. To test this hypothesis, a group of rat hearts was treated with Ang II in the absence or presence of an NADPH oxidase inhibitor, apocynin; or a cell-permeable ROS scavenger, N-acetyl cysteine (NAC). Ang II pretreatment improved postischemic ventricular recovery; reduced myocardial infarction; and decreased the number of cardiomyocyte apoptosis, indicating its ability to precondition the heart against ischemic injury. Both apocynin and NAC almost abolished the preconditioning ability of Ang II. Ang II resulted in increase in ROS activity in the heart, which was reduced by either NAC or apocynin. Ang II also increased both the NADPH oxidase subunits gp91 phox and p22phox mRNA expression, which was abolished with apocynin and NAC. Our results thus demonstrate that the Ang II preconditioning was associated with enhanced ROS activities and increased NADPH oxidase subunits p22phox and gp91phox expression. Both NAC and apocynin reduced ROS activities simultaneously abolishing preconditioning ability of Ang II, suggesting that Ang II preconditioning occurs through redox cycling. That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways.

Authors+Show Affiliations

Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16456238

Citation

Das, Samarjit, et al. "Angiotensin Preconditioning of the Heart: Evidence for Redox Signaling." Cell Biochemistry and Biophysics, vol. 44, no. 1, 2006, pp. 103-10.
Das S, Engelman RM, Maulik N, et al. Angiotensin preconditioning of the heart: evidence for redox signaling. Cell Biochem Biophys. 2006;44(1):103-10.
Das, S., Engelman, R. M., Maulik, N., & Das, D. K. (2006). Angiotensin preconditioning of the heart: evidence for redox signaling. Cell Biochemistry and Biophysics, 44(1), 103-10.
Das S, et al. Angiotensin Preconditioning of the Heart: Evidence for Redox Signaling. Cell Biochem Biophys. 2006;44(1):103-10. PubMed PMID: 16456238.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin preconditioning of the heart: evidence for redox signaling. AU - Das,Samarjit, AU - Engelman,Richard M, AU - Maulik,Nilanjana, AU - Das,Dipak K, PY - 2006/2/4/pubmed PY - 2006/4/6/medline PY - 2006/2/4/entrez SP - 103 EP - 10 JF - Cell biochemistry and biophysics JO - Cell Biochem Biophys VL - 44 IS - 1 N2 - Angiotensin II (Ang II) has been found to exert preconditioning-like effect on mammalian hearts. Diverse mechanisms are known to exist to explain the cardioprotective abilities of Ang II preconditioning. The present study hypothesized, based on the recent report that Ang II generates reactive oxygen species (ROS) through NADPH oxidase, that Ang II preconditioning occurs through redox cycling. To test this hypothesis, a group of rat hearts was treated with Ang II in the absence or presence of an NADPH oxidase inhibitor, apocynin; or a cell-permeable ROS scavenger, N-acetyl cysteine (NAC). Ang II pretreatment improved postischemic ventricular recovery; reduced myocardial infarction; and decreased the number of cardiomyocyte apoptosis, indicating its ability to precondition the heart against ischemic injury. Both apocynin and NAC almost abolished the preconditioning ability of Ang II. Ang II resulted in increase in ROS activity in the heart, which was reduced by either NAC or apocynin. Ang II also increased both the NADPH oxidase subunits gp91 phox and p22phox mRNA expression, which was abolished with apocynin and NAC. Our results thus demonstrate that the Ang II preconditioning was associated with enhanced ROS activities and increased NADPH oxidase subunits p22phox and gp91phox expression. Both NAC and apocynin reduced ROS activities simultaneously abolishing preconditioning ability of Ang II, suggesting that Ang II preconditioning occurs through redox cycling. That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways. SN - 1085-9195 UR - https://www.unboundmedicine.com/medline/citation/16456238/Angiotensin_preconditioning_of_the_heart:_evidence_for_redox_signaling_ L2 - https://dx.doi.org/10.1385/CBB:44:1:103 DB - PRIME DP - Unbound Medicine ER -