Korean J Physiol Pharmacol.
1997 Feb;1(1):45-53.
Gene expression of intrarenal renin-angiotensin system in
streptozotocin-induced diabetic rats
- Affiliations
-
- 1Department of Physiology, School of Medicine, Kyungpook National University.,
Taegu 700-422 South Korea.
Abstract
-
In humans and many animal models with chronic progressive renal
diseases, angiotensin-converting enzyme (ACE) inhibitor markedly
attenuates the progression of nephropathy. Several studies have
reported augmented gene expression and redistribution of renal renin in
partial nephrectomized rats. Although precise mechanism(s) is not
known, the renin-angiotensin system (RAS) may play an important role in
the progression of renal diseases. Thus, this study was undertaken to
examine the gene expression of renal renin, angiotensinogen, and AT-1
subtypes (AT-1A and AT-1B) in rats with diabetic nephropathy, and the
influences of lipopolysaccharide (LPS)-induced septicemia on the gene
expression. Four weeks after streptozotocin (STZ) treatment (55 mg/kg,
i.p.), rats were randomly divided into LPS-treated (1.6 mg/kg, i.p.)
and control rats. At 6 hours after LPS treatment, the rats were killed
and the kidney was removed from each rat. Northern blot and reverse
transcription-polymerase chain reaction (RT-PCR) techniques were used
to detect mRNA expression. STZ treatment markedly attenuated body
weight gain and significantly increased blood glucose level. Renal
renin content (RRC) was significantly decreased in the STZ-treated rats
compared to that in control rats. The renal ACE activity between
STZ-treated and control rats was not significantly different. Renal
renin mRNA level was prominently increased, while angiotensinogen and
AT-1A mRNA levels were slightly decreased in STZ-treated rats compared
to those in controls. AT-1B mRNA level did not differ in both groups.
Acute LPS treatment did not show any significant changes of mRNA levels
of intrarenal RAS components in both groups. These results suggest that
intrarenal RAS components were differentially regulated in STZ-treated
diabetic rats. Further studies are required to evaluate the
relationship between intrarenal RAS and other vasomodulatory systems.