Why the study?
Does renal denervation prevent or reverse hypertension in rats with low-sodium, one-kidney hypertension?
Does renal denervation prevent or reverse hypertension in rats with low-sodium, one-kidney hypertension?
Renal denervation prevents and reverses mild hypertension in a low-sodium, one-kidney rat model, highlighting the role of renal nerves and the renin-angiotensin system in this form of hypertension.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications; leaves open renal nerve mechanisms in experimental hypertension models.
This study examined the role of the renal nerves in both the maintenance and developmental phases of hypertension produced by sodium restriction in one-kidney rats. Results indicate that mild hypertension is sustained through 6 wk after unilateral nephrectomy in rats fed a sodium-deficient diet, with the greatest increase in systolic blood pressure occurring within the first 2 wk. Six weeks after nephrectomy, renal denervation was performed in the sodium-restricted, hypertensive rats, and the blood pressure returned to normotensive levels. Plasma renin activity (PRA) was elevated fourfold after 6 wk of sodium restriction and was unchanged by renal denervation. In another series of experiments that examined the development of hypertension in this experimental model, contralateral renal denervation was performed at the time of nephrectomy, and this prevented the subsequent development of hypertension. PRA was significantly attenuated in these low-sodium, renal-denervated rats that failed to become hypertensive when compared with PRA in hypertensive low-sodium, sham-denervated rats. Kidney norepinephrine content was reduced by 96% after renal denervation in both phases of the hypertension. These data demonstrate that intact renal nerves are necessary for both the development and maintenance of mild hypertension after sodium restriction in one-kidney rats. The pressor contribution of the renal nerves to the hypertension in this experimental model appears to be related, at least in part, to the activation of the renin-angiotensin pressor mechanism.
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Vari et al. (1986) studied this question.
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