The permissive role of nitric oxide in 2 adrenoceptor mediated
dilations in rat cerebral arteries.
Bryan, Robert M., M. L. Steenberg, M. Y. Eichler, T. D. Johnson, M. W.
G. Swafford, M. S. Suresh.
Department of Anesthesiology, Baylor College of Medicine Room 434D,
One Baylor Plaza, Houston, TX 77030
APStracts 2:0308H, 1995.
Dilations produced with UK14,304, a selective 2 adrenoceptor agonist,
in rat middle cerebral arteries (MCAs) were blocked after removal of
the endothelium or inhibition of nitric oxide synthase (NOS). After
endothelium removal or inhibition of NOS, the addition of
subthreshold doses of an exogenous nitric oxide (NO) donor, SNAP,
restored the dilations produced by UK14,304. In a similar manner the
cGMP analogues, 8 bromo-cGMP and dibutyryl-cGMP, restored the
dilations of MCAs after endothelial removal. Since NO cannot be
synthesized and released in MCAs after inhibition of NOS, it cannot
be directly responsible for the dilation. The basal release of NO
from the endothelium acts permissively in the vasodilation by
maintaining adequate levels of cGMP. Removal of this basal release of
NO by removal of endothelium or inhibition of NOS abolishes the 2
adrenoceptor mediated dilation.
Received 8 May 1995; accepted in final form 10 July 1995.
APS Manuscript Number H439-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.