Why the study?
Does arterial baroreceptor denervation affect sodium balance and arterial pressure in rats during varying dietary sodium intake?
Does arterial baroreceptor denervation affect sodium balance and arterial pressure in rats during varying dietary sodium intake?
Arterial baroreceptor denervation impairs the ability to establish sodium balance during both low and high dietary sodium intake and leads to increased arterial pressure during high sodium intake.
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Baroreceptor denervation disrupts sodium balance in rats; leaves open relevance to human salt-sensitive hypertension.
During chronic increased dietary sodium intake, arterial baroreceptors buffer against sustained increases in arterial pressure, and renal sympathoinhibition contributes importantly to the maintenance of sodium balance by decreasing renal tubular sodium reabsorption and increasing urinary sodium excretion. The present study examined the effect of arterial baroreceptor denervation on sodium balance in conscious rats during low, normal, and high dietary sodium intake. Compared with measurements made before arterial baroreceptor denervation, arterial baroreceptor-denervated rats had similar sodium balance during normal dietary sodium intake but significantly more negative sodium balance during low dietary sodium intake and significantly more positive sodium balance during high dietary sodium intake. At the end of the high dietary sodium intake period, arterial pressure (under anesthesia) was 159+/-5 mm Hg after arterial baroreceptor denervation and 115+/-1 mm Hg before arterial baroreceptor denervation. Sham arterial baroreceptor denervation in time control rats had no effect on sodium balance or arterial pressure during the different dietary sodium intakes. These studies indicate that (1) arterial baroreceptor denervation impairs the ability to establish sodium balance during both low and high dietary sodium intake, and (2) arterial baroreceptor denervation leads to the development of increased arterial pressure during high dietary sodium intake in association with increased renal sodium retention.
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DiBona et al. (2002) studied this question.
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