Key result
Intravenous infusion of L-NAME in anesthetized cats caused significant increases in mean arterial blood pressure that were reversed by suppression of peripheral sympathetic nerve activity.
Why the study?
Does systemic inhibition of NO synthesis reveal that NO's vasodilator effects are mediated by inhibition of sympathetic vasoconstriction in anesthetized cats?
Population
Anesthetized cats (n=16 total; 6 baroreceptor-intact, 10 completely baroreceptor-denervated)
Comparison
Intravenous infusion of NG-nitro-L-arginine… vs Baseline states and different experimental…
Design
Preclinical
Authors
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Hypothesis-generating for NO-sympathetic interactions in vivo; requires confirmation in conscious models before clinical relevance.
Does systemic inhibition of NO synthesis reveal that NO's vasodilator effects are mediated by inhibition of sympathetic vasoconstriction in anesthetized cats?
The vasodilator effects of nitric oxide in vivo are largely explained by its inhibition of vasoconstriction caused by peripheral sympathetic nerve activity.
Zanzinger et al. (1994) studied Experimental variation of sympathetic nerve activity (n=16). L-NAME (NG-nitro-L-arginine methyl ester) vs. Baseline was evaluated on Mean arterial blood pressure (MAP). Intravenous infusion of L-NAME in anesthetized cats caused significant increases in mean arterial blood pressure that were reversed by suppression of peripheral sympathetic nerve activity.
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