Show simple item record

dc.contributor.author Ming, Z
dc.contributor.author Han, C
dc.contributor.author Lautt, WW
dc.date.accessioned 2008-01-21T18:27:08Z
dc.date.available 2008-01-21T18:27:08Z
dc.date.issued 2000-01-31
dc.identifier.citation 0008-4212; CAN J PHYSIOL PHARMACOL, JAN 2000, vol. 78, no. 1, p.36 to 44. en
dc.identifier.uri http://hdl.handle.net/1993/3012
dc.description.abstract We previously reported that sympathetic nerve-induced vasoconstriction in the intestine resulted in shear stress induced release of nitric oxide (NO) that led to presynaptic inhibition of transmitter release. In contrast, studies in the liver suggested a postsynaptic inhibition of vascular responses, thus leading to the hypothesis tested here that maintained catecholamine release in the liver would result in maintained metabolic catecholamine action in the face of inhibition of vascular responses. In rats, norepinephrine (NE) induced elevations in arterial glucose content were inhibited by NO synthase antagonism (N-omega-nitro-L-arginine methyl ester (L-NAME), 10 mg/kg, intraportal) but potentiated by NO donor administration (3-morpholinosydnonimine (SIN-1), 0.2 mg/kg, intraportal). The potentiated effect of SIN-1 was abolished by indomethacin (7.5 mg/kg, intraportal). To confirm the hepatic site of metabolic effect, cats were used so that blood flow and hepatic glucose balance could be determined. SIN-1 potentiated NE-induced glucose output from the liver from 5.0 +/- 0.4 to 7.2 +/- 0.6 mg.min(-1.)kg(-1). The potentiation was blocked by methylene blue, a guanylate cyclase inhibitor. Contrary to the glucose response, L-NAME potentiated but SIN-1 attenuated NE-induced portal vasoconstriction. Thus NO is shown to produce differential modulation of vascular and metabolic effects of NE. Vasoconstriction of the hepatic vasculature is inhibited by NO, whereas the glycogenolytic response to NE is potentiated, responses that are probably mediated by prostaglandin. en
dc.format.extent 242780 bytes
dc.format.mimetype application/pdf
dc.language.iso en_US
dc.rights No part of the NRC Research Press electronic journals may be reproduced, stored, or transmitted in any form or by any means, without the written permission of the publisher, except as stated below. Under the Canadian Copyright Act, individuals may download or print single copies of articles for personal research or study. Any person may reproduce short excerpts from articles in the journals for any purpose that respects the moral rights of authors, provided that the source is fully acknowledged. As a courtesy, the consent of authors of such material should be obtained directly from the author. Authorization to reproduce items for other than personal research or study, as stated above, may be obtained via Access © upon payment of the copyright fee of $10.00 per copy. NRC Research Press also extends certain additional rights to authors. The above rights do not extend to copying or reproduction for general distribution, for advertising or promotional purposes, for creating new collective works, or for resale. For such copying or reproduction, arrangements must be made with NRC Research Press. en
dc.subject prostaglandin en
dc.subject glucose en
dc.subject portal vasculature en
dc.subject N-omega-nitro-L-arginine methyl ester en
dc.subject 3-morpholinosydnonimine en
dc.subject PERFUSED-RAT-LIVER en
dc.subject ENDOTHELIAL-CELLS en
dc.subject HEPATOCYTES en
dc.subject GLYCOGENOLYSIS en
dc.subject MODULATION en
dc.subject INSULIN en
dc.subject METABOLISM en
dc.subject RESISTANCE en
dc.subject DECREASE en
dc.subject SHOCK en
dc.title Nitric oxide inhibits norepinephrine-induced hepatic vascular responses but potentiates hepatic glucose output en
dc.status Peer reviewed en
dc.identifier.doi http://dx.doi.org/10.1139/y99-113


Files in this item

This item appears in the following Collection(s)

Show simple item record

View Statistics