Wahab, Nor Akmal
(2004)
Association of malondialdehyde(mda) level and renal impairment in spontaneously hypertensive rats.
Association of malondialdehyde (mda) level and renal impairment in spontaneously hypertensive rats.
(Submitted)
Abstract
Compared to normotensives, hypertensives and patients with renal failure have
higher levels of plasma malondialdehyde (MDA) and unnary 8-epi-prostaglandin F2a.
The exact significance of the raised levels of :MD A and urinary 8-epi-prostaglandin F2a
activity in hypertension is unclear. It is however unclear if they are involved in the
pathogenesis of hypertension or are a consequence of hypertension. This study attempts
to ascertain the age at which changes in blood pressure, levels of plasma 1\IDA, urinary
8-epi-prostaglandin F2a and renal impairment begin to occur in Spontaneously
I-Iypertensive rats (SHR).
Sixty-six, 8-week old Spontaneously Hypertensive Rats (SHR) were divided
equally into eleven groups with age-matched Wistar-Kyoto rats (WKY) as controls.
Every 4 weeks, blood pressure was recorded by the tail-cuff method on six SHR and six
WKY rats. After the measurement of blood pressure, the rats were then individually
housed in metabolic cages for collection of 24-hr urine samples for 8-epi-prostaglandin
. F2a and urine electrolyte determinations and from 36 to 48 weeks onwards for the
measurement of food and water intake. After the urine collection the rats were
anaesthetised for measurement of glomerular filtration rate (GFR) using a standard 3Hinulin
clearance protocol. Immediately upon completion of the measurement of
glomerular filtration rate, the animals were exsanguinated for the determination of plasma
malondialdehyde levels.
Mean body weight of SHR was consistently and significantly lower than that of
WKY rats from the age of 12 weeks onwards (p<O.Ol). Systolic blood pressure was
significantly higher in the SHR when compared to those in age-matched WKY rats from
the age of 8 weeks onwards (p<O.Ol). Plasma MDA and urinary 8-epi-prostaglandin F2a
were all significantly higher in SHR when compared to the controls from the age of 16
and 12 weeks onwards respectively (p<0.05 for :MDA; p<O.Ol for 8-epi-prostaglandin
F2a). GFR was significantly lower (p<0.05) in SHR from the age of 28 weeks onwards
when compared with age-matched normotensive WKY rats. No significant differences
were noted in plasma creatinine concentrations between the two groups throughout the
study period.
In conclusion, it seems, evidence for increased free radical activity appears four to
six weeks after the development of hypertension in SHR rather than the cause of it. In
addition, as renal impairment only becomes evident after changes in free radical activity,
increased free radical activity might have a role in some of the complications associated
with hypertension.
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