Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

Nomura, Gakushi; Takabatake, Toshikazu; Arai, Shigeaki; Uno, Denji; Shimao, M; Hattori, Noriaki

doi:10.1152/ajprenal.1977.232.1.f16

Cited by 5 publications

(2 citation statements)

References 3 publications

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“…Stimulation of renal sympathetic nerves or renal arterial infusion of NE enhance renal tubular reabsorp tion of sodium independent of changes in renal hemody namics [41][42], Renal denervation in the anesthetized rat [43] and dogs [44][45] increased urine volume and urine sodium excretion while GFR and RBF remained unchanged and fractional and absolute sodium and water reabsorption decreased in the proximal tubule. Studies in conscious animals have shown that intact renal innervation is neces sary for normal renal adaptation to sodium restriction [46][47][48][49][50].…”

Section: Discussionmentioning

confidence: 99%

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

et al. 1992

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Since calcium plays a modulatory role in the activity of the sympathetic nervous system (SNS), in these studies, we have tested the hypothesis that hypercalcemia may alter renal SNS activity, and, consequently, renal function. Acute hypercalcemia was induced in Sprague-Dawley rats by infusion of calcium 30mg/kg/2h in 0.45% saline. A control group of rats received only 0.45 % saline. Two more groups of rats received either calcium or 0.45 % saline 7-10 days after total renal denervation. Calcium infusion increased serum calcium by 1.8 ± 0.23 mg/dl in rats with intact renal nerves and by 2.7 ± 0.48 mg/dl in renal denervated rats. Mean arterial pressure and inulin clearance did not change during calcium or 0.45% saline in rats with intact renal nerves. Renal sympathetic nerve activity (RSNA) decreased by 44% in rats infused with calcium, but it did not change in control animals. Calcium caused a significantly greater rise in urine volume, sodium excretion and fractional excretion of sodium than the infusion of 0.45% saline. Rats with renal denervation manifested greater baseline urine volume, sodium excretion and fractional excretion of sodium than rats with intact renal nerves. Infusion of calcium, however, caused no further rise in urine sodium excretion in these animals. α-Methyltyrosine, an inhibitor of norepinephrine (NE) synthesis, also increased natriuresis in rats. Calcium reduced by 27% the NE content in the kidney but not in the heart. Methyltyrosine, on the other hand, reduced NE content in both the heart and the kidney. These data demonstrate that acute hypercalcemia inhibits RSNA and increases diuresis and natriuresis in the absence of any change in blood pressure or in glomerular filtration rate.

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Section: Discussionmentioning

confidence: 99%

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

et al. 1992

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“…On the other hand, the evidence provided by Nomora et al 37 shows that rsna primarily affects the proximal tubule sodium reabsorption, hence it seems plausible to exclude the effects of rsna on sodium reabsorption at other parts of the renal tubular system. The effect of rsna on fractional proximal sodium reabsorption (γ rsna ) has been modeled by curve fitting to the data provided in 8 and 35 [Eq.…”

Section: Proposed Modelmentioning

confidence: 97%

Long-Term Mathematical Model Involving Renal Sympathetic Nerve Activity, Arterial Pressure, and Sodium Excretion

et al. 2005

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This paper presents a physiological long-term model of the cardiovascular system. It integrates the previous models developed by Guyton, Uttamsingh and Coleman. Additionally it introduces mechanisms of direct effects of the renal sympathetic nerve activity (rsna) on tubular sodium reabsorption and renin secretion in accordance with experimental data from literature. The resulting mathematical model constitutes the first long-term model of the cardiovascular system accounting for the effects of rsna on kidney functions in such detail. The objective of developing such a model is to observe the consequences of long-term rsna increase and impairment of rsna inhibition under volume loading. This model provides an understanding of the rsna-related mechanisms, which cause mean arterial pressure increase in hypertension and total sodium amount increase (sodium retention) in congestive heart failure, nephrotic syndrome and cirrhosis.

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The role of the adrenergic nervous system in sodium and water excretion

Güllner

1983

Klin Wochenschr

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There is considerable evidence that the renal nerves contribute to the regulation of salt and water excretion by a direct effect on tubular reabsorption, independent of changes in renal hemodynamics. Whereas the effect of the adrenergic nervous system on sodium reabsorption appears to be established in anesthetised animals, it has been suggested that the basal activity of the renal sympathetic nerves in conscious dogs is too low to have a significant effect on sodium reabsorption by the proximal tubules. However, denervation natriuresis and diuresis has recently been demonstrated in conscious euvolemic and conscious volume expanded rats. The effects of renal nerve stimulation on the handling of sodium and water by the proximal tubule can be mimicked by infusion of the alpha-adrenergic agonist norepinephrine and prevented by infusion of an alpha-adrenergic antagonist. This confirms that it is mediated by alpha-receptors. The adrenergic nervous system may have an independent role in the control of sodium excretion or may be complementary to other systems such as the renin-angiotensin-aldosterone system.

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Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

Cited by 5 publications

References 3 publications

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

Effect of Hypercalcemia on Renal Sympathetic Nervous System Activity

Long-Term Mathematical Model Involving Renal Sympathetic Nerve Activity, Arterial Pressure, and Sodium Excretion

The role of the adrenergic nervous system in sodium and water excretion

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