(Hypertension. 1997;30:35-41.)
© 1997 American Heart Association, Inc.
Articles |
Regulation of Vascular Type 1 Angiotensin Receptors by Cytokines
From the Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Correspondence to Hiroyuki Sasamura, MD, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan.
Abstract Although various cytokines are known to be
expressed in atherosclerotic lesions, it is not known how these
cytokines affect receptors for the peptide hormone
angiotensin II (Ang II). We therefore examined the effects
of interleukin-1
(220 U/mL [10 ng/mL]), tumor necrosis factor-
(280 U/mL [100 ng/mL]), and interferon gamma (100 U/mL) on Ang II
type 1 (AT1) receptors expressed in rat vascular smooth
muscle cells. Treatment with interleukin-1 caused a 1.4- to 1.7-fold
increase in AT1 binding after 24 hours (P<.01)
and a 2.3-fold increase in AT1 mRNA (P<.05).
Tumor necrosis factor- and interferon gamma did not cause a
significant change in AT1 binding when administered alone
but caused a 30% reduction in binding when administered together
(P<.05). The maximal decrease in AT1 binding
(60%, P<.01) was seen with the combination of
interleukin-1 with tumor necrosis factor- and interferon gamma.
Although the upregulation of AT1 by interleukin-1 was
unaffected by pretreatment of cells with
N-monomethyl-L-arginine or
indomethacin, downregulation of AT1 by
interleukin-1 combined with tumor necrosis factor-/interferon
gamma was inhibited by
N-monomethyl-L-arginine
(P<.01). Interleukin-1 treatment enhanced Ang
II–induced [3H]uridine incorporation, whereas treatment
with interleukin-1 combined with tumor necrosis
factor-/interferon gamma attenuated Ang II–induced
[3H]uridine and [3H]leucine incorporation.
These results demonstrate that interleukin-1 upregulates
AT1 receptors and enhances Ang II–stimulated hypertrophic
responses. However, a combination of interleukin-1 with tumor
necrosis factor- and interferon gamma downregulates AT1
receptors by a nitric oxide–dependent mechanism and reduces Ang
II–stimulated trophic responses in vascular smooth muscle cells.
Key Words: angiotensin • receptors, angiotensin • cytokines • interleukin-1 • tumor necrosis factor • interferons
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