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1 Institute of Health Sciences, Quinta da Granja, Monte da Caparica, 2825 Portugal, Spain; and 2 Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0W3
The effect of shear stress on nitric oxide
(NO)-mediated suppression of sympathetic nerve (2-6 Hz)- and
norepinephrine (0.5 µg · kg
1 · min1)-induced
vasoconstriction in the hepatic artery (HA) and portal vein (PV) was
studied using a perfusion circuit to regulate blood pressure and flow
in the cat liver in situ. Holding flow constant resulted
in increased shear stress during constriction; holding pressure steady
prevented changes in shear stress. When shear stress was allowed to
rise, the vasoconstriction (indicated by elevation in perfusion
pressure) in response to nerve stimulation and norepinephrine was
significantly potentiated after NO synthase blockade using
NG-nitro-L-arginine methyl ester
(L-NAME, 2.5 mg/kg iv) in both the HA and PV (response to nerves: HA control 28.8 ± 6.5 mmHg, L-NAME 62.7 ± 14.6 mmHg; PV
control 1.5 ± 0.5 mmHg,
L-NAME 3.3 ± 0.5 mmHg; response to norepinephrine: HA control 32.4 ± 9.0 mmHg, L-NAME 60.3 ± 8.0 mmHg; PV control 1.3 ± 0.3 mmHg,
L-NAME 3.4 ± 0.7 mmHg). The
potentiation was reversed by
L-arginine (75 mg/kg). When
shear stress was held constant by maintaining constant perfusion
pressure, L-NAME did not cause
potentiation of vasoconstriction. The data are consistent with the
hypothesis that elevated shear stress in the hepatic blood vessels
leads to NO-dependent postjunctional modulation of vasoconstriction.
shear stress; neuromodulation; blood flow; portal pressure
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