Selective renal denervation guided by renal nerve stimulation: mapping renal nerves for unmet clinical needs

2019 ◽  
Vol 33 (10) ◽  
pp. 716-724 ◽  
Author(s):  
Kunyue Tan ◽  
Yinchuan Lai ◽  
Weijie Chen ◽  
Hang Liu ◽  
Yanping Xu ◽  
...  
Hypertension ◽  
2019 ◽  
Vol 74 (3) ◽  
pp. 536-545 ◽  
Author(s):  
Hang Liu ◽  
Weijie Chen ◽  
Yinchuan Lai ◽  
Huaan Du ◽  
Zihao Wang ◽  
...  

2002 ◽  
Vol 282 (6) ◽  
pp. F1043-F1048 ◽  
Author(s):  
Albert Quan ◽  
Michel Baum

The proximal tubule synthesizes and secretes angiotensin II into the lumen, where it regulates transport. Renal denervation abolishes the effect of angiotensin II on proximal tubule transport. Using in vivo microperfusion, we examined whether renal nerve stimulation modulates the effect of angiotensin II on transport. The effect of angiotensin II was assessed by measuring the decrease in volume reabsorption with the addition of 10−4M luminal enalaprilat. Luminal enalaprilat did not alter volume reabsorption (2.80 ± 0.18 vs. 2.34 ± 0.14 nl · mm−1 · min−1). However, with renal nerve stimulation, enalaprilat decreased volume reabsorption (3.45 ± 0.22 vs. 1.67 ± 0.20 nl · mm−1 · min−1, P < 0.0005). The absolute and percent decrements in volume reabsorption with luminal enalaprilat were higher with renal nerve stimulation than with native innervation (1.78 ± 0.19 vs. 0.46 ± 0.23 nl · mm−1 · min−1, P < 0.02, and 51.8 ± 5.0 vs. 14.6 ± 7.4%, P < 0.05, respectively). Renal nerve stimulation did not alter the glomerular filtration rate or renal blood flow. Renal nerve stimulation augments the stimulatory effect of intraluminal angiotensin II. The sympathetic renal nerves modulate the proximal tubule renin-angiotensin system and thereby regulate proximal tubule transport.


2018 ◽  
Vol 27 (5) ◽  
pp. 271-279 ◽  
Author(s):  
Mark R. de Jong ◽  
Annemiek F. Hoogerwaard ◽  
Ahmet Adiyaman ◽  
Jaap Jan J. Smit ◽  
Jan-Evert Heeg ◽  
...  

1983 ◽  
Vol 244 (1) ◽  
pp. E52-E60 ◽  
Author(s):  
U. Kopp ◽  
T. Bradley ◽  
P. Hjemdahl

The effect of renal nerve stimulation (RNS) on renal venous outflow and urinary excretion of endogenous norepinephrine, epinephrine, and dopamine was examined in anesthetized dogs. In the unstimulated denervated kidney, there was a negative venoarterial concentration difference for all catecholamines. Low-level RNS (LLRNS) caused small changes in renal hemodynamics and renal venous outflow of dopamine and increased norepinephrine outflow by 3.22 +/- 0.95 pmol X min-1 X g-1 (n = 5, P less than 0.05). High-level RNS (HLRNS) reduced renal blood flow by 50% and increased renal venous outflow of norepinephrine and dopamine by 9.58 +/- 0.67 and 0.46 +/- 0.05 pmol X min-1 X g-1, respectively (n = 27, P less than 0.01 for both). Renal uptake of epinephrine was unchanged by HLRNS. The urinary excretion of norepinephrine but not dopamine was increased to a similar degree following RNS at both levels. HLRNS caused a similar increase of the urinary norepinephrine excretion from the contralateral denervated and unstimulated kidney. This could be explained by the increase in arterial norepinephrine (from 0.74 +/- 0.08 to 1.20 +/- 0.14 nM, P less than 0.01) caused by HLRNS as shown by experiments with intravenous infusions of norepinephrine. The alpha-adrenoceptor antagonist phenoxybenzamine counteracted the hemodynamic response to HLRNS and enhanced the renal venous outflow and urinary excretion of norepinephrine and dopamine. Our results indicate that renal nerves release dopamine as well as norepinephrine and that urinary catecholamine excretion is a poor indicator of intrarenal catecholamine release.


1980 ◽  
Vol 238 (6) ◽  
pp. H770-H775 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody

Renal hypertension is accompanied by alterations in the renal sympathetic innervation involving reduced catecholamine content and histofluorescence. Because the renal nerves are a potentially important factor in the pathogenesis of renal hypertension, the functional significance of renal catecholamine depletion was evaluated. In rats with either one-kidney or two-kidney Grollman hypertension, renal vascular responses to renal nerve stimulation and intraarterial administration of vasoactive hormones were assessed in vivo at various times following renal compression. In the wrapped kidney of one-kidney hypertensive rats, vasoconstrictor responses to renal nerve stimulation were consistently reduced, compared to responses in uninephrectomized control rats, whereas responses to intra-arterial norepinephrine were slightly greater in kidneys from hypertensive animals. In the untouched kidney of rats with two-kidney renal hypertension, vasoconstrictor responses to nerve stimulation were also substantially reduced, although those to norepinephrine were only slightly altered. It was concluded that catecholamine depletion in the kidneys of renal hypertensive animals reflects a diminished capacity of renal sympathetic nerve impulses to produce vasoconstriction. Reduced neurogenic renal vascular resistance may serve to attenuate the rise in blood pressure in renal hypertension.


Hypertension ◽  
2016 ◽  
Vol 67 (6) ◽  
pp. 1211-1217 ◽  
Author(s):  
Mark R. de Jong ◽  
Annemiek F. Hoogerwaard ◽  
Pim Gal ◽  
Ahmet Adiyaman ◽  
Jaap Jan J. Smit ◽  
...  

1980 ◽  
Vol 239 (4) ◽  
pp. F371-F377 ◽  
Author(s):  
Juan A. Oliver ◽  
John Pinto ◽  
Robert R. Sciacca ◽  
Paul J. Cannon

In order to determine whether the fraction of norepinephrine released from the renal nerves that escapes into the circulation can be used an an index of renal sympathetic nervous activity, arterial and renal vein plasma norepinephrine concentrations were measured by a radioenzymatic technique along with renal blood flow in anesthetized dogs under control conditions and during electrical renal nerve stimulation. In 25 animais studied under conditions of normal sodium balance, plasma norepinephrine in the renal vein, 198 ± 26 pg/ml, was significantly higher than in arterial blood, 102 ± 10 pg/ml (P < 0.001). In five dogs, electrical stimulation of the renal nerves (12 V, 3 ms) at frequencies of 0.5, 2,6, 12, and 18 Hz for 1 min was associated with increased norepinephrine concentration in renal venous plasma and an increase in the calculated renal norepinephrine overflow. There was a significant linear relationship between the frequency of stimulation and norepinephrine overflow into the renal vein in each animal, but there was also a significant interanimal variation in the slope of this relationship (P <0.01). Electrical stimulation at a frequency of 2 Hz significantly decreased renal blood flow (-24 ± 7 ml/min, P < 0.01). The maximal effect was achieved at 6 Hz (-66 ± 11 ml/min). The data indicate that there is a base-line overflow of norepinephrine into the renal venous blood of the dog that increases with increasing frequency of electrical nerve stimulation. They suggest that measurements of norepinephrine overflow into the renal vein may be used to assess the activity of the renal sympathetic nervous system. renal blood flow; catecholamines; renin; dog Submitted on January 10, 1980 Accepted on April 29, 1980


Hypertension ◽  
2016 ◽  
Vol 68 (3) ◽  
pp. 707-714 ◽  
Author(s):  
Mark R. de Jong ◽  
Ahmet Adiyaman ◽  
Pim Gal ◽  
Jaap Jan J. Smit ◽  
Peter Paul H.M. Delnoy ◽  
...  

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