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Attenuating effect of Heme Oxygenase induction by Stannous Chloride on salt‐induced hypertension in male Sprague‐Dawley rats
Author(s) -
Oloyo Ahmed Kolade,
Ochie Daniela Ogochukwu,
Bello Nurudeen Adebowale,
Elias Simiat Olanike,
Sofola Olusoga Adekunle
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.708.1
Subject(s) - heme oxygenase , blood pressure , medicine , endocrinology , chemistry , heme , nitrite , bilirubin , saline , biochemistry , enzyme , nitrate , organic chemistry
Heme oxygenase (HO) is implicated in the regulation of blood pressure both under normal and pathological conditions. Impaired vascular function leading to heightened vascular resistance is one of the mechanisms by which a high salt diet (HSD) elevates blood pressure. This study evaluated the effect of heme oxygenase induction by stannous chloride (50mg/kg body weight s.c for 4 days) on the response of BP to vasoactive substances in male Sprague‐Dawley rats fed a normal salt or high salt (0.3% and 8% NaCl) diet respectively for 6 weeks. Rats fed a HSD showed increases in arterial blood pressure (BP) [123 ± 5 vs. 102 ± 4], fluid balance (FB) [12.8 ± 1.23 vs. 6.78 ± 1.02], that was accompanied by decreased plasma concentration of bilirubin [0.84 ± 0. 11 vs. 1.36 ± 0.14] and nitrite [0.32 ±0.03 vs. 0.86 ± 0.04]. HO induction reduced the increment in BP [107 ± 5 vs. 123 ± 5] and FB [5.74 ± 0.98 vs. 12.8 ± 1.23] while restoring both bilirubin [1.30 ± 0.12 vs. 0.84 ± 0.11] and nitrite [0.70 ± 0.06 vs. 0.32 ± 0.03] level towards that of control. Likewise HO induction attenuated the blunted change in MABP in response to cumulative i.v PE and ACh that was observed in rats fed a HSD. However, change in MABP in response to i.v SNP was similar across the groups. Induction of HO via s.c stannous chloride administration attenuates blood pressure elevating effect of a HSD by mechanisms involving maintenance of FB and interactions between bilirubin and NO pathways.