Why the study?
Does bilateral renal denervation improve renal sodium handling and reduce renal damage in spontaneously hypertensive rats?
Does bilateral renal denervation improve renal sodium handling and reduce renal damage in spontaneously hypertensive rats?
Bilateral renal denervation increases sodium excretion and reduces histological markers of renal damage in a rat model of spontaneous hypertension.
Animal data suggest potential renal benefits; leaves open translation to human hypertension management.
Renal sympathetic nerve activity has an important role in renal disease-associated hypertension and in the modulation of fluid homeostasis. In the present study, changes in renal function and renal sodium/potassium handling were investigated in groups of 12-week-old male, spontaneously hypertensive rats with renal denervation (RDNX group) or sham denervation (sham group). The RDNX group excreted significantly more sodium than the sham group during the 2-week observation period (P<0.05). Following bilateral renal denervation, the fractional lithium excretion was elevated in the RDNX group compared with the sham group, but no significant effect was observed of renal denervation on the fractional distal reabsorption rate of sodium or the fractional excretion of potassium. Furthermore, the glomerular injury score and the wall-to-lumen ratio of the interlobular artery were significantly lower in the RDNX group than in the sham group (P<0.05). In conclusion, the present study indicates an involvement of the renal sympathetic nerves in the regulation of renal tubular sodium reabsorption in spontaneously hypertensive rats and in the renal damage associated with hypertension.
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Li et al. (2016) studied this question.