Hypertension, Vol 17, 881-887, Copyright © 1991 by American Heart Association
PJ Lacolley, SJ Lewis and MJ Brody
The aim of the present study was to examine the involvement of the
sympathetic nervous system in the generation or release of vascular nitric
oxide. In urethane-anesthetized rats, the administration of the novel
nitric oxide synthesis inhibitor L-N-nitro arginine (LNA) (0.02 mmol/kg
i.v.) increased mean arterial pressure and renal, mesenteric, and
hindquarter vascular resistances. The intravenous administration of
L-arginine (60 mg/kg plus 12 mg/kg/min i.v.) produced small reductions in
arterial pressure and vascular resistances and abolished the hemodynamic
effects of LNA. Pretreatment with the ganglion blocking agent
chlorisondamine lowered mean arterial pressure and vascular resistances,
abolished the LNA-induced pressor and renal vasoconstrictor response, and
attenuated the increases in mesenteric and hindquarter resistances. In
contrast, the vasodilator hydralazine lowered mean arterial pressure and
vascular resistances to levels equivalent to that of ganglionic blockade;
however, the subsequent administration of LNA still produced significant
increases in arterial pressure and regional vascular resistances. In
ganglion-blocked rats in which pressure and vascular resistances were
returned to normal levels by infusion of arginine vasopressin or
phenylephrine, the pressor and vasoconstrictor effects of LNA were
restored. However, phenylephrine was significantly more efficacious and
markedly exaggerated the action of LNA. These results suggest that the
sympathetic nervous system plays an important role in modulating the
synthesis or release of vascular nitric oxide through the effects of 1)
normal sympathetic discharge, 2) humoral activation of alpha-adrenergic
receptors, and 3) vascular tone per se.
ARTICLES
Role of sympathetic nerve activity in the generation of vascular nitric oxide in urethane-anesthetized rats
Department of Pharmacology, University of Iowa College of Medicine, Iowa City.
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