title: Short-term use of telmisartan attenuates oxidation and improves Prdx2 expression more than antioxidant β-blockers in the cardiovascular systems of spontaneously hypertensive rats.
abstract: Reactive oxygen species (ROS) and antioxidant enzymes are required to maintain homeostasis. The loss of this balance can cause excessive ROS production and damage to the cardiovascular tissues. Angiotensin II receptor blockers (ARBs) and β-blockers with antioxidant effects may inhibit ROS in the cardiovascular system. In this study, we directly compared the effects of ARBs and β-blockers with antioxidant properties on cardiovascular protection and the regulation of endothelial progenitor cell (EPC) numbers in the setting of oxidative stress in hypertensive rats. To compare the effects of the drugs, animals were divided into the following groups: Wistar-Kyoto rats (WKY), untreated spontaneously hypertensive rats (SHR) and SHR treated with tempol (TEMP, 5 mg kg(-1) per day), trichlorothiazide (TCTZ, 1.6 mg kg(-1) per day), atenolol (25 mg kg(-1) per day), nebivolol (NEBL, 5 mg kg(-1) per day), carvedilol (CVDL, 30 mg kg(-1) per day) or telmisartan (TERT, 5 mg kg(-1) per day). Following 2 weeks of treatment, blood pressures (BPs) and aortic wall thicknesses were similarly reduced in each antihypertensive drug-treated group. Superoxide anion and malondialdehyde levels were significantly reduced following treatment with NEBL, CVDL and TERT. Additionally, the expression levels of NADPH oxidase subunits were also reduced in the TERT-, CVDL- and NEBL-treated groups. Furthermore, these drugs improved both EPC numbers and the expression levels of peroxiredoxin 2 (Prdx2), an antioxidant enzyme, in the heart and kidneys but not the aorta. Cardiac Prdx2 expression, in particular, was markedly improved by TERT, NEBL and CVDL treatment, and renal Prdx2 expression was enhanced by TEMP. Our data indicate that short-term treatment with TERT may have more beneficial effects on cardiovascular protection, EPC number improvements and Prdx2 expression compared with CVDL and NEBL. In conclusion, TERT may positively modulate the balance between oxidative stress and antioxidant properties and demonstrate capabilities beyond its BP-lowering effects.
authors.affiliation: 1] Laboratory of Cardiovascular Regeneration, Division of Cardiovascular Medicine, Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea [2] Department of Biomedical Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
authors.forename: Sae Mi
authors.initials: SM
authors.lastname: Yoo
authors.affiliation: 1] Laboratory of Cardiovascular Regeneration, Division of Cardiovascular Medicine, Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea [2] Department of Biomedical Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
authors.forename: Sung Hyun
authors.initials: SH
authors.lastname: Choi
authors.affiliation: Department of Biochemistry, University of Rochester, Rochester, NY, USA.
authors.forename: Monica Dha Yea
authors.initials: MD
authors.lastname: Jung
authors.affiliation: Division of Clinical Pharmacy, College of Pharmacy, The Catholic University of Korea, Bucheon, Republic of Korea.
authors.forename: Sung Cil
authors.initials: SC
authors.lastname: Lim
authors.affiliation: 1] Laboratory of Cardiovascular Regeneration, Division of Cardiovascular Medicine, Seoul St Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea [2] Department of Biomedical Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
authors.forename: Sang Hong
authors.initials: SH
authors.lastname: Baek
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism; D001562:Benzimidazoles / Q000494:pharmacology*; D001565:Benzoates / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D006321:Heart / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D054464:Peroxiredoxins / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013481:Superoxides / Q000378:metabolism; D000077333:Telmisartan
chemical_list: D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D000975:Antioxidants; D001562:Benzimidazoles; D001565:Benzoates; D013481:Superoxides; D008315:Malondialdehyde; D054464:Peroxiredoxins; D000077333:Telmisartan