Vol. 173, No. 2, 1990
December 14, 1990
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Pages 541-547
DEXAMETHASONE PREVENTS THE INDUCTION BY ENDOTOXlN OF A
NITRIC OXIDE SYNTHASE AND THE ASSOCIATED
EFFECTS ON VASCULAR TONE: AN INSIGHT INTO ENDOTOXlN SHOCK
D.D. Rees, S. Cellek, R.M.J. Palmer and S. Moncada
Wellcome Research Laboratories
Langley Court, Beckenham, Kent BR3 3BS, United Kingdom
Received October 19, 1990
Summary: The relationship between vascular tone and the induction by
endotoxin of a nitric oxide (NO) synthase was studied in vitro in rings of
rat thoracic aorta. In rings with and without endothelium there was a
time-dependent induction of NO synthase accompanied by both spontaneous
and L-arginine-induced relaxation and by reduced contractility to
phenylephrine. These effects, which were attributable to the presence of
endotoxin in the Krebs' buffer, were attenuated by cycloheximide, polymyxin
B and inhibitors of NO synthase. Furthermore, dexamethasone inhibited the
induction of NO synthase and the consequent effects on vascular tone.
These findings indicate that prevention of the induction of NO synthase by
glucocorticoids may be an important component of their therapeutic action.
©1990 Academic Press, Inc.
Nitric oxide (NO) synthesized from L-arginine by the vascular
endothelium plays a role in the physiological regulation of blood flow and
blood pressure (1). In this and other tissues, such as the brain, adrenal
gland and platelets, NO is produced by a synthase which is constitutive,
Ca 2+-, and NAD PH-dependent ( 1,2-4). However, in macrophages,
neutrophils, Kupffer cells and hepatocytes (5-7) NO is produced by an
2+
enzyme which is Ca -independent, and is induced by endotoxin (LPS) and
cytokines. This NO plays a role in host defence mechanisms, for it is
cytotoxic for bacteria, protozoa, fungi and tumour cells (8). Other roles for
this NO have not been defined, however, excessive production of
immunologically derived NO may be responsible for the hypotension and the
reduced responses to pressor agents (9) characteristic of endotoxin shock.
L-arginine, which has little or no effect on the tone of freshly isolated
rings of vascular tissue, produces a substantial relaxation of rings of rat
aorta and bovine pulmonary artery incubated for 6 and 24 h respectively in
vitro. This action, which is endothelium-independent, has been attributed
to depletion of L-arginine during prolonged incubation (10, 11).
We have, however, shown that the vascular endothelium expresses an
inducible, Ca2+-independent NO synthase after activation in vitro with LPS
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