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Autocrine effects of endothelin-1 on leukocyte-endothelial interaction:
stimulation of endothelin B receptor subtype reduces endothelial
adhesiveness via a nitric oxide-dependent mechanism
T Murohara and AM Lefer
Department of Physiology, Jefferson Medical College, Thomas Jefferson
University, Philadelphia, PA 19107-6799, USA.
The effects of endothelin-1 (ET-1) on P-selectin-mediated leukocyte
endothelial interaction were examined in vitro. Adherence of autologous
polymorphonuclear leukocytes (PMNs) to the endothelium was markedly
enhanced by endothelial stimulation with either (2 U/mL) thrombin, (1
mumol/L) histamine, or (100 nmol/L) phorbol myristate acetate (PMA). In
contrast, ET-1 alone (10 and 100 nmol/L) only slightly increased the number
of adhering PMNs. The increased PMN adherence to thrombin- or
histamine-stimulated endothelium, which was blocked by an anti-P- selectin
monoclonal antibody, was also significantly attenuated by preincubation of
coronary segments with (100 nmol/L) ET-1. We further investigated the
mechanism of this anti-adherence action of ET-1 on thrombin-stimulated
endothelial adhesiveness. Preincubation of coronary segments with a
selective ETA receptor antagonist, BQ485 (1 mumol/L), had no effect on ET-1
inhibition of thrombin-induced PMN adherence. In contrast, preincubation
with a selective ETB receptor antagonist, BQ788 (1 mumol/L) significantly
reversed ET-1 inhibition of thrombin-induced PMN adherence, whereas the
selective ETB receptor agonist BQ-3020 mimicked the inhibitory action of
ET-1 on thrombin-induced PMN adherence. Furthermore, (100 mumol/L) N
omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS)
inhibitor, significantly attenuated ET-1 inhibition of thrombin-stimulated
PMN adherence. These results suggest that ET-1 may inhibit
P-selectin-mediated leukocyte- endothelial interaction via ETB receptor
stimulation and subsequent endothelial NO formation. This autocrine effect
of ET-1 may be involved in pathophysiologic states such as early
atherogenesis by preventing leukocyte-endothelial interaction in
constricted blood vessels.
Volume 88,
Issue 10,
pp. 3894-3900,
11/15/1996
Copyright © 1996 by The American Society of Hematology
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