Nitric oxide-dependent and -independent norepinephrine release in
rat mesenteric arteries.
Yamamoto, Ryuichi, Akihiko Wada, Yujiro Asada, Toshihiko Yanagita,
Tomoaki Yuhi, Hiromi Niina, Akinobu Sumiyoshi, Hideyuki Kobayashi,
and Tony J. F. Lee.
Departments of Pharmacology and Pathology, Miyazaki Medical
College, 5200 Kihara, Kiyotake, Miyazaki 889-16, Japan, Department of
Pharmacology, Southern Illinois University School of Medicine, P.O.
Box 19230, Springfield, Illinois 62794-9230, U.S.A.
APStracts 3:0374H, 1996.
The role of nitric oxide (NO) on endogenous norepinephrine (NE)
release in the perfused, isolated rat mesenteric vasculature was
examined. NE overflow elicited by electrical field stimulation (EFS)
at various frequencies was significantly smaller at 24 C than at 37
C. The pressor response upon EFS at 8 and 10 Hz, however, was higher
at 24 C than at 37 C. When production of NO was blocked by Nw-nitro
-L-arginine (L-NNA), NE overflow upon EFS at each frequency of
stimulation was diminished by 50% at 37 C but remained unchanged at
24 C, while the pressor response elicited by EFS became greater at 37
C than at 24 C. These effects of L-NNA were reversed by L- arginine,
but not by its D-enantiomer. Sodium nitroprusside, an NO donor,
increased EFS-elicited NE overflow at 24 C, but had no effect at 37
C. These results demonstrate that NE release is both NO-dependent and
NO- independent. The NO-dependent mechanism is more sensitive to
cooling than is the NO-independent mechanism. The increase in EFS
-elicited perfusion pressure at 24 C may be due to reduction in
synthesis of NO (a potent vasodilator), thus unmasking the effect of
NE and other non-catecholamine vasoconstrictors.
Received 12 September 1995; accepted in final form 24 July 1996.
APS Manuscript Number H856-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996