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Adrenergic modulation of human polymorphonuclear leukocyte activation.
Potentiating effect of adenosine
G Bazzoni, E Dejana and A Del Maschio
Laboratory of Vascular Biology, Istituto di Ricerche Farmacologiche Mario
Negri, Milano, Italy.
The activation of polymorphonuclear leukocytes (PMN) is an important step
in the development of tissue damage associated with inflammatory and
ischemic conditions. Catecholamines have been reported to inhibit PMN
functions, but the high concentrations required cast doubt on their actual
relevance as a defense mechanism. We report here that adenosine, which is
actively released in ischemic conditions, potentiates the effect of
epinephrine and reduces the minimal active concentration required to
inhibit PMN activation by at least two orders of magnitude. Epinephrine
caused a dose-related reduction of chemiluminescence, superoxide anion
generation, enzyme release (lysozyme and beta- glucuronidase), and adhesion
to endothelial cell (EC) monolayers in human PMN activated by
N-formyl-methionyl-leucyl-phenyl-alanine (fMLP). This effect was only
apparent at 10(-7) to 10(-6) mol/L. As expected, adenosine caused
dose-dependent reductions of superoxide anion production and PMN adhesion
to EC. Adenosine and epinephrine combined had an additive effect on PMN
superoxide production and adhesion to EC. The minimal effective
concentration of epinephrine in combination with 10(-8) mol/L adenosine was
in the range of 10(-10) to 10(-9) mol/L. In contrast, adenosine inhibited
only slightly enzyme release and did not significantly enhance the
inhibition by epinephrine on this parameter. Studies with adenosine analogs
suggested that the potentiating effect of adenosine was mediated by A2
receptors. The mechanism of potentiation was not related to additive effect
on intracellular cyclic adenosine monophosphate levels. Epinephrine's
ability to modulate PMN activation and the potentiating effect of adenosine
may constitute a form of physiologic protection against tissue injury in
inflammatory and ischemic processes.
Volume 77,
Issue 9,
pp. 2042-2048,
05/01/1991
Copyright © 1991 by The American Society of Hematology
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