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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


APOCYNIN PREVENTS REACTIVE OXYGEN SPECIES PRODUCTION AND IMPROVES NITRIC OXIDE AVAILABILITY IN THE EXPERIMENTAL HYPERTENSION
Abstract number: PTH10-83

Jendekova1 L., Kojsova1 S., Pechanova1 O.

1Institute of Normal and Pathological Physiology SAS, Bratislava, Slovak Republic; [email protected]

Aim: 

The purpose of this study was to investigate the preventive effect of NADPH oxidase inhibitor – apocynin (4-hydroxy-3-methoxyacetophenone) on the development of systolic blood pressure (SBP) in borderline hypertensive rats (BHR) and spontaneously hypertensive rats (SHR).

Methods: 

Young 6-week-old male BHR (offspring of SHR dams and Wistar Kyoto sires) and SHR were treated with apocynin (30 mg/kg/day) for six weeks. SBP was measured by tail-cuff plethysmography. Nitric oxide synthase (NOS) activity was determined in the left ventricle and aorta. Protein expression of nuclear factor kappaB (NF-kB) and NAD(P)H oxidase subunits p67phox and p22phox as well as concentration of cGMP were determined in the left ventricle.

Results: 

Apocynin significantly decreased SBP in all groups investigated. Administration of apocynin had no effect on NOS activity in either tissue studied. However, apocynin lowered protein expression of the NF-kB in all groups, decreased protein expression of NAD(P)H oxidase subunit p22phox in both hypertensive groups and attenuated protein expression of the NAD(P)H oxidase subunit p67phox in SHR. Moreover, apocynin was able to prevent lowering of concentration of cGMP in the left ventricle of both hypertensive groups.

Conclusion: 

Our study demonstrated that apocynin treatment partially prevented SBP rise in borderline and spontaneously hypertensive rats without increasing activity of NOS in the left ventricle and aorta. However, apocynin was able to decrease production of reactive oxygen species in hypertensive rats and thus to prevent cGMP decrease.

The study was supported by VEGA 2/6148/26

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PTH10-83

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