Why the study?
Does renal denervation improve sodium and water excretion in stroke-prone spontaneously hypertensive rats?
Does renal denervation improve sodium and water excretion in stroke-prone spontaneously hypertensive rats?
Renal sympathetic nerve activity contributes to the reduced water and sodium excretion in stroke-prone spontaneously hypertensive rats when renal perfusion pressure is normalized.
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Supports sympathetic contribution to renal impairment in this model; leaves open clinical translation of renal denervation.
In stroke-prone spontaneously hypertensive rats (SHRSP), urinary excretion of sodium and water and glomerular filtration rate (GFR) are markedly decreased by acute normalization of the renal perfusion pressure using an aortic clamping technique. To examine the mechanism for the decreased sodium and water excretion, SHRSP rats were subjected to bilateral renal denervation. Sodium and water excretion and GFR in SHRSP with aortic clamping were significantly restored by the renal denervation. The restoration was more prominent in the urine flow and GFR. When renal perfusion pressure was normalized by administration of sympatholytic drugs in another group of SHRSP, sodium and water excretion were decreased. However, the extent of the decrease in urine flow but not in sodium excretion was significantly less than that in SHRSP with aortic constriction. GFR was not changed by administration of the sympatholytic drugs. Renal denervation lowered the blood pressure in SHRSP. These results suggest that renal sympathetic nerve activity is greatly involved in the reduced water excretion and partly involved in the reduced sodium excretion in SHRSP rats.
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Nagaoka et al. (1982) studied this question.
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