Our previous studies have provided evidence for the existence of an intrins
ic renin-angiotensin system (RAS) in the rat pancreas, which may play a rol
e in the regulation of pancreatic microcirculation and ductal secretion. Su
ch a pancreatic RAS has recently shown to be activated by chronic hypoxia.
The activation of a local RAS ill the pancreas by chronic hypoxia and its s
ignificance of changes may be important for the physiological and pathophys
iological aspects of the pancreas. In the present study, the regulation of
experimentally induced acute pancreatitis on the expression of local RAS in
the pancreas was investigated using Western blot, semi-quantitative revers
e transcription-polymerase chain reaction (RT-PCR) and immunohistochemical
approaches. Results from Western blot demonstrated that experimentally indu
ced pancreatitis caused significantly increased expression of the pancreati
c RAS component proteins. In keeping with the protein level, RT-PCR analysi
s also revealed the enhanced expression of pancreatic RAS genes, notably th
e angiotensinogen in experimental pancreatitis. Immunohistochemical results
Further demonstrated that increased immunoreactivity for RAS in experiment
al pancreatitis was predominantly localized to the endothelia and epithelia
of pancreatic vasculature and ductal system respectively. The data indicat
e that experimental pancreatitis may elicit activation of a local RAS in th
e pancreas. Such an activation of pancreatic RAS and its significance of di
fferential changes in individual RAS components could play a role in the pa
thophysiology of acute pancreatitis (C) 2000 Elsevier Science Ireland Ltd.
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