Potentiation to vasodilators by nitric oxide synthase blockade in
superior mesenteric but not hepatic artery.
Macedo, M. Paula, and W. Wayne Lautt.
DEPARTMENT OF PHARMACOLOGY & THERAPEUTICS, FACULTY OF MEDICINE,
UNIVERSITY OF MANITOBA, WINNIPEG, MANITOBA, CANADA, R3E OW3
APStracts 3:0208G, 1996.
It was our objective to determine the vasodilator effect of adenosine
and isoproterenol on the hepatic (HA) and superior mesenteric (SMA)
artery before and after blockade of NO production to evaluate the
possibility of organ specificity. Vascular circuits supplied blood
flow to the liver or intestine in cats under sodium pentobarbital
anesthesia. The NO synthase antagonist, NG-nitro-L-arginine methyl
ester (L-NAME) (2.5 mg x kg-1, i.v.), increased arterial pressure
from 106.4 + 7.6 mmHg to 141.4 + 8.1 mmHg and raised basal vascular
tone in the SMA but not the HA. The NO synthase substrate, L-arginine
(75 mg x kg-1), reversed these effects. The decrease in perfusion
pressure in response to adenosine was 51.7 + 2.9, 135.2 + 6.1, and
16.7 + 2.4 mmHg respectively for control, and after L-NAME and L
-arginine. Isoproterenol was also potentiated in the SMA. Adenosine
and isoproterenol were not potentiated in the HA by L-NAME.
Potentiation did not occur when HA or SMA basal tone was elevated by
norepinephrine. In conclusion, L-NAME increased basal tone for the
SMA and potentiated the dilation induced by adenosine and
isoproterenol in the SMA but not in the HA. This study provides
evidence that there is a highly organ-specific compensatory mechanism
in which the absence of nitric oxide promotes potentiation of other
vasodilators.
Received 10 May 1996; accepted in final form 16 September 1996.
APS Manuscript Number G189-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996