Why the study?
Does renal denervation prevent the increase in arterial pressure in Wistar rats with aortic depressor nerve transection?
Does renal denervation prevent the increase in arterial pressure in Wistar rats with aortic depressor nerve transection?
In a rat model, renal denervation prevents hypertension induced by aortic nerve transection by altering central sympathetic outflow, suggesting a key role for afferent renal nerves.
Answers are grounded in this paper and cite their sources.
Renal denervation may blunt sympathetic hypertension after baroreflex loss in rats; hypothesis-generating for human afferent nerve mechanisms.
The role of renal nerves in influencing the control of arterial pressure was studied in Wistar rats with aortic depressor nerve (ADN) transection. Renal denervation prevented or reversed the normal increase in arterial pressure seen after ADN transection. This effect was not due to an effect on the renin-angiotensin system, as the elevated arterial pressure after ADN section in rats with renal nerves intact was shown to be due to increased alpha-adrenergic activity. Food and water intake and urine output decreased significantly in both renal-denervated and sham-denervated rats after ADN section, suggesting that a pressure diuresis mechanism was not responsible for preventing the rise in pressure in renal-denervated rats. In another study, the concentration of norepinephrine in skeletal muscle and hypothalamus at 0 and 8 hours after inhibition of tyrosine hydroxylase with alpha-methyltyrosine was used as an index of norepinephrine turnover. Norepinephrine turnover in skeletal muscle was increased significantly over control values by ADN transection in sham renal-denervated rats, but was not significantly different from controls in renal-denervated rats with ADN section. In the hypothalamus, there was a significant difference between the turnover of norepinephrine in the two groups of ADN-sectioned rats. The results taken together suggest that renal denervation prevents the arterial pressure response to ADN transection by altering the central mechanisms governing sympathetic outflow. It is suggested that this effect may be due to elimination of information carried by afferent renal fibers.
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Kline et al. (1983) studied this question.
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