Key result
Intracerebroventricular clonidine lowers MAP by ~22 mm Hg via nitric oxide release.
Why the study?
The study was designed to determine whether the hypotensive action of clonidine results from its stimulation of excess nitric oxide in the brain.
Does clonidine's central hypotensive action require nitric oxide production in the brain in rat models?
Population
In vitro brain slices and in vivo anesthetized rats
Comparison
Clonidine stimulation vs basal state and NO production blockade
Design
Preclinical experimental study
Authors
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Hypothesis-generating for NO mediation of clonidine's central action in rats; extends preclinical mechanisms but should not change practice.
Does clonidine's central hypotensive action require nitric oxide production in the brain in rat models?
Clonidine's central antihypertensive effect is mediated by the stimulation of nitric oxide release in the brain.
Dobrucki et al. (2001) studied this question. Clonidine vs. Basal state / NO blockade with L-NAME was evaluated on Nitric oxide concentration in the nucleus tractus solitarius, mean arterial pressure, and heart rate. Intracerebroventricular infusion of clonidine increased NO concentration in the nucleus tractus solitarius and decreased mean arterial pressure by 22 mm Hg, an effect reduced by NO blockade.
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