Korean J Physiol Pharmacol.
1997 Apr;1(2):151-159.
Effect of hemorrhage on mRNA expressions of renin, angiotensinogen and
AT-1 receptors in rat central and peripheral tissues
- Affiliations
-
- 1
Department of Physiology, School of Medicine, Kyungpook National University
,101 Tong-in 2 Ka,Chungku, Taegu 700-422 South Korea.
Abstract
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In an attempt to investigate whether hemorrhage affects the gene
expression of the renin-angiotensin system (RAS) components in the
brain and peripheral angiotensin-generating tissues, changes in mRNA
levels of the RAS components in response to hemorrhage were measured in
conscious unrestrained rats. Wistar rats were bled at a rate of 3
ml/kg/min for 5 min, and then decapitated 7 h after hemorrhage. Levels
of mRNA for renin, angiotensinogen and angiotensin II-AT-1 receptor
subtypes (AT-1A and AT-1B) were determined with the methods of northern
blot and reverse transcriptase-polymerase chain reaction (RT-PCR).
Hemorrhage produced a profound hypotension with tachycardia, but blood
pressure and heart rate recovered close to the basal level at 7 h.
Plasma and renal renin levels were significantly increased at 7 h.
Hemorrhage induced rapid upregulation of gene expression of both AT-1A
and AT-1B receptor subtypes in the brainstem and hypothalamus,
downregulation of them in the adrenal gland and liver. However, renin
mRNA level increased in the brainstem, decreased in the liver, but was
not changed in the hypothalamus, kidney and adrenals after hemorrhage.
Angiotensinogen mRNA level was not significantly changed in any of the
tissue except a slight increase in the liver. The kidney and liver did
not show any significant change in gene expression of the RAS
components. These results suggest that gene expression of the RAS in
central and peripheral tissues are, at least in part, under independent
control and the local RAS in each organ plays specific physiologic
role.