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Vol. 290, Issue 3, 1409-1416, September 1999
Department of Chemistry, An increase in arginase activity has been associated with the
pathophysiology of a number of conditions, including an impairment in
nonadrenergic and noncholinergic (NANC) nerve-mediated relaxation of
the gastrointestinal smooth muscle. An arginase inhibitor may rectify
this condition. We compared the effects of a newly designed arginase
inhibitor, 2(S)-amino-6-boronohexanoic acid (ABH), with the currently available
N
-hydroxy-L-arginine
(L-HO-Arg), on the NANC nerve-mediated internal anal
sphincter (IAS) smooth-muscle relaxation and the arginase activity in
the IAS and other tissues. Arginase caused an attenuation of the
IAS smooth-muscle relaxations by NANC nerve stimulation that was
restored by the arginase inhibitors. L-HO-Arg but not ABH
caused dose-dependent and complete reversal of
N-nitro-L-arginine-suppressed
IAS relaxation that was similar to that seen with
L-arginine. Both ABH and L-HO-Arg caused an
augmentation of NANC nerve-mediated relaxation of the IAS. In the IAS,
ABH was found to be 
250 times more potent than L-HO-Arg
in inhibiting the arginase activity. L-HO-Arg was found to
be 10 to 18 times more potent in inhibiting the arginase activity in
the liver than in nonhepatic tissues. We conclude that arginase plays a
significant role in the regulation of nitric oxide synthase-mediated
NANC relaxation in the IAS. The advent of new and selective arginase inhibitors may play a significant role in the discrimination of arginase isozymes and have important pathophysiological and therapeutic implications in gastrointestinal motility disorders.
0022-3565/99/2903-1409$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics
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