Impaired neurogenic control of renal vasculature in renal hypertensive rats

1980 ◽  
Vol 238 (6) ◽  
pp. H770-H775 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Innervation ◽  
Renal Hypertension ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Renal Vascular ◽  
Renal Sympathetic

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.

Basal norepinephrine overflow into the renal vein: effect of renal nerve stimulation

1980 ◽  
Vol 239 (4) ◽  
pp. F371-F377 ◽  
Author(s):  
Juan A. Oliver ◽  
John Pinto ◽  
Robert R. Sciacca ◽  
Paul J. Cannon
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Nerve Stimulation ◽  
Renal Vein ◽  
Renal Nerves ◽  
Plasma Norepinephrine ◽  
Renal Nerve ◽  
Sympathetic Nervous ◽  
Renal Nerve Stimulation ◽  
Renal Sympathetic

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

Renal vascular resistance and reactivity in the spontaneously hypertensive rat

1979 ◽  
Vol 237 (2) ◽  
pp. F128-F132 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Renal Vascular Resistance ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Wide Range ◽  
Renal Nerve Stimulation ◽  
Renal Vascular

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30––100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.

Effect of renal nerve stimulation on responsiveness of the rat renal vasculature

2002 ◽  
Vol 283 (5) ◽  
pp. F1056-F1065 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Nerve Stimulation ◽  
Low Frequency ◽  
Rectangular Pulse ◽  
Signal Frequency ◽  
Renal Nerves ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Low Frequency Oscillations ◽  
Renal Nerve Stimulation

When the renal nerves are stimulated with sinusoidal stimuli over the frequency range 0.04–0.8 Hz, low (≤0.4 Hz)- but not high (≥0.4 Hz)-frequency oscillations appear in renal blood flow (RBF) and are proposed to increase responsiveness of the renal vasculature to stimuli. This hypothesis was tested in anesthetized rats in which RBF responses to intrarenal injection of norepinephrine and angiotensin and to reductions in renal arterial pressure (RAP) were determined during conventional rectangular pulse and sinusoidal renal nerve stimulation. Conventional rectangular pulse renal nerve stimulation decreased RBF at 2 Hz but not at 0.2 or 1.0 Hz. Sinusoidal renal nerve stimulation elicited low-frequency oscillations (≤0.4 Hz) in RBF only when the basal carrier signal frequency produced renal vasoconstriction, i.e., at 5 Hz but not at 1 Hz. Regardless of whether renal vasoconstriction occurred, neither conventional rectangular pulse nor sinusoidal renal nerve stimulation altered renal vasoconstrictor responses to norepinephrine and angiotensin. The RBF response to reduction in RAP was altered by both conventional rectangular pulse and sinusoidal renal nerve stimulation only when renal vasoconstriction occurred: the decrease in RBF during reduced RAP was greater. Sinusoidal renal nerve stimulation with a renal vasoconstrictor carrier frequency results in a decrease in RBF with superimposed low-frequency oscillations. However, these low-frequency RBF oscillations do not alter renal vascular responsiveness to vasoconstrictor stimuli.

Renal nerve stimulation augments effect of intraluminal angiotensin II on proximal tubule transport

2002 ◽  
Vol 282 (6) ◽  
pp. F1043-F1048 ◽  
Author(s):  
Albert Quan ◽  
Michel Baum
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Nerve Stimulation ◽  
Filtration Rate ◽  
Renin Angiotensin System ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Angiotensin System ◽  
Renal Nerve Stimulation

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.

Losartan corrects abnormal frequency response of renal vasculature in congestive heart failure

2003 ◽  
Vol 285 (5) ◽  
pp. H1857-H1863 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Frequency Response ◽  
Nerve Stimulation ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Pass Filter ◽  
Vasoconstrictor Response ◽  
Renal Nerve Stimulation

In congestive heart failure, renal blood flow is decreased and renal vascular resistance is increased in a setting of increased activity of both the sympathetic nervous and renin-angiotensin systems. The renal vasoconstrictor response to renal nerve stimulation is enhanced. This is associated with an abnormality in the low-pass filter function of the renal vasculature wherein higher frequencies (≥0.01 Hz) within renal sympathetic nerve activity are not normally attenuated and are passed into the renal blood flow signal. This study tested the hypothesis that excess angiotensin II action mediates the abnormal frequency response characteristics of the renal vasculature in congestive heart failure. In anesthetized rats, the renal vasoconstrictor response to graded frequency renal nerve stimulation was significantly greater in congestive heart failure than in control rats. Losartan attenuated the renal vasoconstrictor response to a significantly greater degree in congestive heart failure than in control rats. In control rats, the frequency response of the renal vasculature was that of a first order (–20 dB/frequency decade) low-pass filter with a corner frequency (–3 dB, 30% attenuation) of 0.002 Hz and 97% attenuation (–30 dB) at ≥0.1 Hz. In congestive heart failure rats, attenuation did not exceed 45% (–5 dB) over the frequency range of 0.001–0.6 Hz. The frequency response of the renal vasculature was not affected by losartan treatment in control rats but was completely restored to normal by losartan treatment in congestive heart failure rats. The enhanced renal vasoconstrictor response to renal nerve stimulation and the associated abnormality in the frequency response characteristics of the renal vasculature seen in congestive heart failure are mediated by the action of angiotensin II on renal angiotensin II AT1 receptors.

Renal venous outflow and urinary excretion of norepinephrine, epinephrine, and dopamine during graded renal nerve stimulation

1983 ◽  
Vol 244 (1) ◽  
pp. E52-E60 ◽  
Author(s):  
U. Kopp ◽  
T. Bradley ◽  
P. Hjemdahl
Keyword(s):  
Urinary Excretion ◽  
Nerve Stimulation ◽  
Renal Nerves ◽  
Similar Degree ◽  
Venous Outflow ◽  
Renal Nerve ◽  
Concentration Difference ◽  
Alpha Adrenoceptor ◽  
Renal Nerve Stimulation ◽  
High Level

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.

Continuous measurement of renal blood flow changes to renal nerve stimulation and intra-arterial drug administration in the rat

1978 ◽  
Vol 234 (2) ◽  
pp. H219-H222 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Renal Artery ◽  
Nerve Stimulation ◽  
Continuous Measurement ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Renal Vascular ◽  
Flow Circuit ◽  
Stimulation Of

A method is described for continuous measurement of renal blood flow in the anesthetized rat without dissection of the renal artery. Blood flow and arterial pressure were measured in an extracorporeal flow circuit between the carotid artery and an aortic pouch from which the left renal artery was the only outlet. Injection into the flow circuit allowed delivery of drugs directly into the arterial blood supply of the kidney. Electrical stimulation of undamaged periarterial renal kidney. Electrical stimulation of undamaged periarterial renal nerves was possible since the renal artery remained undisturbed. Extracorporeal autoperfusion of the rat kidney produced renal flow and resistance measurements that did not differ from those obtained with a flow probe placed directly on the renal artery. Renal nerve stimulation was found to cause renal vasoconstriction due to activation of alpha-adrenergic receptors by norepinephrine released from postganglionic sympathetic neurons. Renal vascular responses to a variety of intra-arterial vasoactive agents were also determined. The method described here allows the evaluation of renal vascular control in the variety of disease states for which suitable rat models have been developed.

Cells of origin of the sympathetic renal innervation in rat

1987 ◽  
Vol 252 (6) ◽  
pp. F957-F963 ◽  
Author(s):  
W. Sripairojthikoon ◽  
J. M. Wyss
Keyword(s):  
Rat Kidney ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Splanchnic Nerve ◽  
Retrograde Transport ◽  
Fluorescent Labeling ◽  
Renal Nerves ◽  
Anatomical Location ◽  
Renal Nerve ◽  
Renal Sympathetic

Physiological studies are rapidly elucidating the function of the renal nerves; however, the anatomical location of the postganglionic cell bodies that supply the rat kidney has not been fully clarified. The origin of the sympathetic projection to the rat kidney was investigated in the present study by use of the fluorescent dye retrograde transport technique. Application of the dye to the renal nerves resulted in the fluorescent labeling of sympathetic cell bodies in paravertebral [thoracic (T) segment 6 through lumbar (L) segment 4] and prevertebral (renal, greater splanchnic, and celiac) ganglia and along the greater splanchnic nerve. Sympathetic neurons in all of these locations were round to fusiform in shape, 16-40 micron in diameter. They were dispersed uniformly throughout the paravertebral ganglia and splanchnic nerve, but in the celiac and greater splanchnic ganglia, cells projecting to the kidney were clustered near the origin of the renal nerve. In contrast to the cat, in which greater than 50% of the renal sympathetic innervation arises from the prevertebral ganglia, in the rat the majority (greater than 70%) of labeled renal sympathetic neurons were in the paravertebral ganglia, especially T12-L1. The distribution of renal sympathetic neurons in the paravertebral ganglia closely approximates the rostrocaudal distribution of renal afferent cell bodies in the dorsal root ganglia.

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 ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Renal Nerve Stimulation
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