Key result
Chronic atrial natriuretic factor infusion suppresses catecholamine excretion in hypertensive rats, signaling sympathetic inhibition.
Why the study?
The mechanisms by which atrial natriuretic factor affects sympathetic nervous activity and natriuresis in the one-kidney, one-clip rat hypertension model were not fully understood.
Does chronic infusion of atrial natriuretic factor suppress sympathetic activity in a one-kidney, one-clip model of rat hypertension?
Does chronic infusion of atrial natriuretic factor suppress sympathetic activity in a one-kidney, one-clip model of rat hypertension?
Atrial natriuretic factor suppresses sympathetic activity in a rat model of hypertension, which may contribute to its natriuretic effect.
ANF natriuresis may involve catecholamine modulation in this rat model; leaves open any human relevance and should not change practice.
The one-kidney, one-clip model of rat hypertension was found to have an increased natriuresis following chronic infusion of atrial natriuretic factor (ANF). We have now found that this natriuretic effect of ANF is associated with a suppression of the initially elevated urinary excretion of norepinephrine and epinephrine and increase of the excretion of the main dopamine metabolite-dihydroxyphenylacetic acid as well as of the urinary dopamine to norepinephrine ratio. These data are compatible with the hypothesis that ANF suppresses the increased sympathetic activity in this model of hypertension and this action combined with opposite changes of dopamine may contribute to the natriuretic effect of ANF.
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Debinski et al. (1986) studied One-kidney, one-clip hypertension (rat model). Atrial natriuretic factor (ANF) was evaluated on Urinary excretion of norepinephrine, epinephrine, and dopamine metabolites. Chronic infusion of atrial natriuretic factor in a rat model of hypertension suppressed elevated urinary excretion of norepinephrine and epinephrine, suggesting inhibition of sympathetic activity.
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