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Glutathione Related Enzyme Activities in Spontaneous Hypertensive Rat Heart

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Title: Glutathione Related Enzyme Activities in Spontaneous Hypertensive Rat Heart
Authors: Diaz, Carlos Manvel / Goto, Shinji / Urata, Yoshishige / Niwa, Masami / Kondo, Takahito / Tsuji, Yoshiro
Issue Date: 30-Jun-1998
Citation: Acta medica Nagasakiensia. 1998, 43(1-2), p.23-28
Abstract: It has been reported that oxygen radicals are involved in the development of tissue injury in hypertension. To prevent o xidative stress, there are antioxidant systems inside the cells such as superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reducatase (GR), catalase (CAT) and glutathione S-transferase (GST). In this study changes in these antioxidant activities were estimated in the outer wall of the left ventricles from spontaneously hypertensive rats (SHR), stroke prone SHR (SHRSP) and normal Wister Kyoto rats (WKY). The activities of manganese-superoxide dismutase (Mn-SOD), which localizes in mitochondria and GST were lower in the left ventricles of SHR and SHRSP compared to those in WKY. Slight decrease in the GPX activity was observed in the left ventricles from SHR and SHRSP. On the other hand, the activity of GR and catalase was not different in them. The effect of Nicardipine, a calcium channel blocker, on these antioxidant activities was also esimated. Treatment of these rats with nicardipine (150 mg/kg/day) for 4 weeks improved blood pressure, from 176ツア10 mmHg to 140ツア8 mmHg in SHR (n = 5), from 201ツア11 mmHg to 167ツア5 in SHRSP (n = 5), respectively, and restored the activities of Mn-SOD, GST and GPX. Collectively, these results suggest that oxidative stress in hypertensive rat heart causes supression of antioxidant activities, which may contribute to myocardical injury, and nicardipine plays a cardioprotective role to reduce the oxidative stress in hypertensive heart.
Keywords: antioxidants / calcium channels / hypertension.
URI: http://hdl.handle.net/10069/16100
ISSN: 00016055
Type: Departmental Bulletin Paper
Text Version: publisher
Appears in Collections:Volume 43, No. 1-2

Citable URI : http://hdl.handle.net/10069/16100

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