Effect of Acute Unilateral Renal Denervation on Intrarenal Haemodynamics and Urinary Excretion in Rats before and during Hypervolaemia

1982 ◽  
Vol 62 (5) ◽  
pp. 457-464 ◽  
Author(s):  
A. T. Veressa ◽  
C. K. Chong ◽  
H. Sonnenberg
Keyword(s):  
Blood Flow ◽  
Renal Denervation ◽  
Flow Distribution ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Blood Volume Expansion ◽  
Anaesthetized Rats ◽  
Renal Nerve Activity ◽  
Sodium And Potassium

1. The possible involvement of renal nerves in the diuresis and natriuresis of blood volume expansion was studied in anaesthetized rats. Acute unilateral renal denervation caused increased excretion of fluid, sodium and potassium. 2. Renal blood and plasma flows were elevated without change in filtration rate. Intracortical blood flow distribution was not affected by the denervation. 3. Blood infusion caused diuresis, natriuresis and kaliuresis in both denervated and shamdenervated kidneys, associated with comparable initial increases in filtration and decreases in renal blood flow. No change in flow distribution was found, whether or not renal nerves were intact. 4. Although the magnitude of the excretory response to hypervolaemia was greater in denervated kidneys, the temporal pattern was identical with that of sham-operated kidneys. Our data thus do not show an effect of efferent renal nerve activity on volume natriuresis.

Functional response to graded increases in renal nerve activity during hypoxia in conscious rabbits

1996 ◽  
Vol 271 (6) ◽  
pp. R1489-R1499 ◽  
Author(s):  
S. C. Malpas ◽  
A. Shweta ◽  
W. P. Anderson ◽  
G. A. Head
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Gas Mixtures ◽  
Renin Activity ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Conscious Rabbits

Changes in renal sympathetic nerve activity (SNA) are postulated to influence renal function in selective ways, such that different levels of activation produce particular renal responses, initially in renin release, then sodium excretion, with changes in renal hemodynamics occurring only with much greater stimulus intensities. The aim of this study was to determine the renal hemodynamic and excretory responses to graded physiological increases in renal SNA induced by breathing different hypoxic gas mixtures. Experiments were performed in seven conscious rabbits subjected to four gas mixtures (14% O2, 10% O2, 10% O2 + 3% CO2, and 10% O2 + 5% CO2) and instrumented for recording of renal nerve activity. After a 30-min control period, rabbits were subjected to one of the four gas mixtures for 30 min, and then room air was resumed for a further 30 min. The four gas mixtures increased renal SNA by 14, 38, 49, and 165% respectively, but arterial pressure (thus renal perfusion pressure) was not altered by any of the gas mixtures. The greatest level of sympathetic activation produced significant falls in glomerular filtration rate (GFR), renal blood flow, sodium and fluid excretion, and significant increases in plasma renin activity. These returned to levels not significantly different from control conditions in the 30-min period after the gas mixture. When the changes to the various gas mixtures were analyzed within each rabbit, a significant linear relationship was found with all variables to the increase in SNA. Renal denervation in a separate group of seven rabbits completely abolished all of the above responses to the different gas mixtures. Thus graded activation of renal nerves induced by changes in inspired gas mixtures resulted in graded decreases in renal blood flow, GFR, and sodium excretion and graded increases in renin activity, with the changes occurring across a similar range of nerve activities; there was no evidence for a selective change in any renal variable.

The Sodium-Retaining Effect of Renal Nerve Activity in the Cat: Role of Angiotensin Formation

1976 ◽  
Vol 51 (1) ◽  
pp. 93-102 ◽  
Author(s):  
E. J. Johns ◽  
Barbara A. Lewis ◽  
Bertha Singer
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Sodium Clearance

1. The effect of low-frequency stimulation of the renal nerves on renal function and renin release has been investigated. The experiments were performed in unilaterally nephrectomized, anaesthetized cats in which the nerves to the remaining kidney were sectioned. 2. When stimulation frequency was adjusted to reduce renal blood flow by approximately 15% for 15 min, glomerular filtration rate was hardly affected. The ratio sodium clearance/glomerular filtration rate was significantly reduced and plasma renin activity was significantly increased. 3. When the renal nerves were similarly stimulated in the presence of the β-adrenergic receptor blocking agent, propranolol, the glomerular filtration rate was significantly reduced and the rise in plasma renin activity was significantly inhibited. The reduction of sodium clearance/glomerular filtration rate was as great as in the control animals. 4. The results are consistent with the view that the maintenance of glomerular filtration rate, during renal nerve stimulation which reduced renal blood flow, may be mediated by the local generation of angiotensin. The results also suggest that angiotensin does not play an important role in the sodium retention associated with increased renal nerve activity.

Effect of renal denervation, furosemide, and acute saline loading on postobstructive diuresis in the rat

1981 ◽  
Vol 59 (1) ◽  
pp. 59-64 ◽  
Author(s):  
D. R. Wilson ◽  
U. Honrath
Keyword(s):  
Filtration Rate ◽  
Renal Denervation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Saline Loading ◽  
Anaesthetized Rats ◽  
Renal Nerve Activity ◽  
Solute Excretion

The effect of acute or chronic renal denervation, furosemide, or acute saline loading on the postobstructive diuresis (POD) which occurs after relief of 24-h bilateral ureteral obstruction (BUO) was studied in anaesthetized rats. Acute renal denervation during POD 1–2 h after relief of BUO had no effect on glomerular filtration rate or sodium, potassium, water, or solute excretion, in contrast with its natriuretic and diuretic effect in sham-operated rats. Intravenous furosemide or acute saline loading caused a further marked increase in sodium and water excretion during POD, demonstrating the ability of the kidney undergoing POD to respond to other types of natriuretic stimuli. Chronic renal denervation prior to BUO had no effect on subsequent POD.The lack of response of the BUO kidney undergoing POD to acute denervation contrasts with the changes in renal function following denervation of the unilateral postobstructive kidney. The results indicate that the kidney undergoing POD after relief of BUO may be functionally denervated and suggest that inhibition of renal nerve activity could contribute to the pathophysiology of POD.

scholarly journals Renal nerves do not mediate vasoconstrictor responses to acute nitric oxide synthesis inhibition in conscious rats.

1997 ◽  
Vol 8 (6) ◽  
pp. 887-892
Author(s):  
C Baylis ◽  
R Braith ◽  
B R Santmyire ◽  
K Engels
Keyword(s):  
Nitric Oxide ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Synthesis Inhibition ◽  
Renal Vasoconstriction ◽  
Vasoconstrictor Response ◽  
Renal Nerve Activity ◽  
Renal Vascular

Nitric oxide is a physiologically important peripheral and renal vasodilator. The studies presented here were conducted in the conscious, chronically catheterized, unstressed rat to investigate whether NO interacts with renal efferent sympathetic nerve activity in control of blood pressure, renal vascular resistance, and sodium excretion. Renal clearance studies were conducted in normal rats with innervated kidneys and in a separate group of rats with chronic, bilateral renal denervation. Acute systemic inhibition of NO synthesis with n-nitro L-arginine methyl ester (L-NAME) leads to hypertension, renal vasoconstriction, and natriuresis in rats with intact renal nerves. Chronic renal denervation does not diminish the pressor and renal vasoconstrictor response to NO synthesis inhibition, although the natriuretic response is prevented. Stimulation of renal NO synthesis with the substrate L-arginine produces selective renal vasodilation and a marked osmotic diuresis in the innervated kidney. Renal denervation has little impact on the responses to L-arginine. These studies suggest that in the normal, conscious, chronically catheterized rat in which the sympathetic nervous system is operating at basal levels, renal nerve activity does not contribute to the pressor or renal vasoconstrictor response to NO inhibition or the renal vasodilator response to NO stimulation. These observations contrast with earlier observations made under conditions of stress-induced activation of renal nerve activity.

Neuronal regulation of renal function: A model system for nervous system interactions

1992 ◽  
Vol 70 (5) ◽  
pp. 733-734 ◽  
Author(s):  
J. Michael Wyss
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Renal Disease ◽  
Easy Access ◽  
Renal Nerves ◽  
Clinical Consequence ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity

The kidney is the most highly innervated peripheral organ, and both the excretory and endocrine functions of the kidney are regulated by renal nerve activity. The kidney plays a dominant role in body fluid homeostasis, blood ionic concentration, and pH and thereby contributes importantly to systemic blood pressure control. Early studies suggested that the neural-renal interactions were responsible only for short-term adjustments in renal function, but more recent studies indicate that the renal nerves may be a major contributor to chronic renal defects leading to established hypertension and (or) renal disease. The neural-renal interaction is also of considerable interest as a model to elucidate the interplay between the nervous system and peripheral organs, since there is abundant anatomical and physiological information characterizing the renal nerves. The investigator has easy access to the renal nerves and the neural influence on renal function is directly quantifiable both in vivo and in vitro. In this symposium that was presented at the 1990 annual convention of the Society for Neuroscience in St. Louis, Missouri, three prominent researchers evaluate the most recent progress in understanding the interplay between the nervous system and the kidney and explore how the results of these studies relate to the broader questions concerning the nervous system's interactions.First, Luciano Barajas examines the detailed anatomy of the intrarenal distribution of the efferent and afferent renal nerves along the nephron and vasculature, and he evaluates the physiological role of each of the discrete components of the innervation. His basic science orientation combined with his deep appreciation of the clinical consequence of the failure of neural-renal regulation enhances his discussion of the anatomy. Ulla C. Kopp discusses the role of the renorenal reflex, which alters renal responses following stimulation of the contralateral kidney. She also considers her recent findings that efferent renal nerve activity can directly modify sensory feedback to the spinal cord from the kidney. Finally, J. Michael Wyss examines the functional consequences of neural control of the kidney in health and disease. Although the nervous system has often been considered as only an acute regulator of visceral function, current studies into hypertension and renal disease suggest that neural-renal dysfunction may be an important contributor to chronic diseases.Together, these presentations examine most of the recent advances in the area of neural-renal interactions and point out how these data form a basis for future research into neuronal interactions with all visceral organs. The relative simplicity of the neural-renal interaction makes this system an important model with which to elucidate all neural-peripheral and neural-neural interactions.

Lack of effect of chronic renal denervation on altered sodium reabsorption during increased ureteral pressure

1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath
Keyword(s):  
Isotonic Saline ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity

The role of the renal nerves in the altered sodium reabsorption which occurs during increased ureteral pressure was studied using clearance techniques in anaesthetized rats undergoing diuresis induced by isotonic saline infusion. In rats with a sham denervated kidney, an ipsilateral increase in ureteral pressure to 20 cm H2O resulted in a marked and significant decrease in sodium and water excretion, increased fractional sodium reabsorption, and increased urine osmolality with no significant change in glomerular filtration rate. A similar significant ipsilateral increase in tubular reabsorption of sodium occurred in rats with chronically denervated kidneys during increased ureteral pressure. The changes in tubular reabsorption were rapidly reversible after return of ureteral pressure to normal. These experiments indicate that enhanced tubular reabsorption of sodium during an ipsilateral increase in ureteral pressure is not mediated by increased renal nerve activity. During the antinatriuresis of increased ureteral pressure there was a decrease in the fractional reabsorption of sodium from the opposite normal kidney. The role of the renal nerves in this compensatory change in function in the opposite kidney was studied in two further groups of animals. The renal response to a contralateral increase in ureteral pressure was similar in denervated and sham-denervated kidneys. The results indicate that altered renal nerve activity, through ipsilateral or contralateral renorenal reflexes, is not responsible for the changes in tubular reabsorption of sodium which occur during increased ureteral pressure induced by partial ureteral obstruction.

Age-dependent changes in afferent renal nerve activity in genetically hypertensive rats

1992 ◽  
Vol 262 (5) ◽  
pp. R834-R841 ◽  
Author(s):  
N. G. Moss ◽  
A. B. Scoltock
Keyword(s):  
Single Unit ◽  
Renal Ischemia ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Wky Rats ◽  
Renal Nerve Activity ◽  
Single Unit Recordings ◽  
Wistar Kyoto

Multiunit and single-unit recordings of afferent renal nerve activity (ARNA) were obtained in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats between 35 and 150 days of age. Intrapelvic backflow of urine at 20 mmHg excited ARNA at all ages in SHR (152 +/- 18% above control) and WKY rats (262 +/- 24%). In SHR, complete renal ischemia was more excitatory in rats older than 120 days (1,233 +/- 103%, n = 8) than in younger SHR (317 +/- 28%, n = 42). Single-unit recordings showed that this was related to the appearance of R1 chemoreceptors in older SHR and coincided with a decline in the proportion of R2 chemoreceptors in the renal nerves. Other chemoreceptive responses were identified in single units that did not show complete R1 or R2 characteristics, some of which showed responses consistent with a transformation process from R2 to R1 receptor type. R1 chemoreceptors were not present in WKY rats studied up to 150 days of age and, unlike SHR, the proportion of R2 chemoreceptors did not decline with age. Accordingly, complete renal ischemia in WKY rats caused a comparable excitation in multiunit ARNA at all ages (285 +/- 33%, n = 43). Oral enalapril from weaning to 100 days of age prevented hypertension in SHR but did not impair the responsiveness of ARNA to any stimulus. In WKY rats, enalapril treatment for the same period resulted in exaggerated ARNA response to renal ischemia (1,250 +/- 377% above control).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal nerves in exaggerated water and sodium excretion by hypertrophied kidney of anesthetized rats

1988 ◽  
Vol 254 (1) ◽  
pp. F32-F37 ◽  
Author(s):  
G. Szenasi ◽  
G. Kottra ◽  
P. Bencsath ◽  
L. Takacs
Keyword(s):  
Thiobarbituric Acid ◽  
Male Rats ◽  
Renal Nerves ◽  
Sham Operation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Before And After ◽  
Renal Nerve Activity ◽  
And Control ◽  
Water And Sodium Excretion

The effect of acute renal denervation (RD) on water (V), sodium (UNaV), and potassium excretion (UKV) from the hypertrophied and control kidney was studied in 5-sec-butyl-5-ethyl-2-thiobarbituric acid (Inactin)-anesthetized male rats 7 days after unilateral nephrectomy (Nx) or sham operation (SNx). V, UNaV, and UKV from the hypertrophied kidney were similar before and after RD or sham RD. In contrast, in SNx rats, left RD resulted in an ipsilateral increase in V (from 2.76 +/- 0.39 to 5.31 +/- 0.99 microliters.min-1.g-1), UNaV (from 109 +/- 36 to 857 +/- 331 nmol.min-1.g-1), and UKV (from 144 +/- 44 to 807 +/- 130 nmol.min-1.g-1; P less than 0.05 in all cases). Moreover, renal parameters from the hypertrophied kidney, subjected to either RD or sham RD, were not different from values after RD in SNx rats (V: Nx, sham RD = 5.72 +/- 1.10; Nx, RD = 5.23 +/- 0.66; SNx, RD = 5.31 +/- 0.99 microliters.min-1.g-1; UNaV: Nx, sham RD = 896 +/- 319; Nx, RD = 821 +/- 262; SNx, RD = 857 +/- 331 nmol.min-1.g-1; UKV: Nx, sham RD = 782 +/- 127; Nx, RD = 860 +/- 82; SNx, RD = 807 +/- 130 nmol.min-1.g-1). In additional experiments, integrated renal nerve activity (RNA) to the kidney in Nx and SNx rats was 4.0 +/- 0.3 and 10.7 +/- 0.9 microV (P less than 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Afferent renal innervation in anti-Thy1.1 nephritis in rats

2020 ◽  
Vol 319 (5) ◽  
pp. F822-F832
Author(s):  
Kristina Rodionova ◽  
Roland Veelken ◽  
Karl F. Hilgers ◽  
Eva-Maria Paulus ◽  
Peter Linz ◽  
...  
Keyword(s):  
Renal Tissue ◽  
In Vitro Assays ◽  
Renal Nerves ◽  
Dual Function ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Cgrp Release ◽  
Renal Nerve Activity

Afferent renal nerves exhibit a dual function controlling central sympathetic outflow via afferent electrical activity and influencing intrarenal immunological processes by releasing peptides such as calcitonin gene-related peptide (CGRP). We tested the hypothesis that increased afferent and efferent renal nerve activity occur with augmented release of CGRP in anti-Thy1.1 nephritis, in which enhanced CGRP release exacerbates inflammation. Nephritis was induced in Sprague-Dawley rats by intravenous injection of OX-7 antibody (1.75 mg/kg), and animals were investigated neurophysiologically, electrophysiologically, and pathomorphologically 6 days later. Nephritic rats exhibited proteinuria (169.3 ± 10.2 mg/24 h) with increased efferent renal nerve activity (14.7 ± 0.9 bursts/s vs. control 11.5 ± 0.9 bursts/s, n = 11, P < 0.05). However, afferent renal nerve activity (in spikes/s) decreased in nephritis (8.0 ± 1.8 Hz vs. control 27.4 ± 4.1 Hz, n = 11, P < 0.05). In patch-clamp recordings, neurons with renal afferents from nephritic rats showed a lower frequency of high activity following electrical stimulation (43.4% vs. 66.4% in controls, P < 0.05). In vitro assays showed that renal tissue from nephritic rats exhibited increased CGRP release via spontaneous (14 ± 3 pg/mL vs. 6.8 ± 2.8 pg/ml in controls, n = 7, P < 0.05) and stimulated mechanisms. In nephritic animals, marked infiltration of macrophages in the interstitium (26 ± 4 cells/mm2) and glomeruli (3.7 ± 0.6 cells/glomerular cross-section) occurred. Pretreatment with the CGRP receptor antagonist CGRP8–37 reduced proteinuria, infiltration, and proliferation. In nephritic rats, it can be speculated that afferent renal nerves lose their ability to properly control efferent sympathetic nerve activity while influencing renal inflammation through increased CGRP release.

Renal effects of volume expansion in the renal-denervated nonhuman primate

1984 ◽  
Vol 247 (6) ◽  
pp. H960-H966
Author(s):  
T. V. Peterson ◽  
N. L. Chase ◽  
D. K. Gray
Keyword(s):  
Nonhuman Primate ◽  
Volume Expansion ◽  
Renal Denervation ◽  
Recovery Period ◽  
Isotonic Saline ◽  
Free Water ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
A Cell

Experiments were performed to determine the role of renal nerves in mediating the renal excretory effects of volume expansion in the nonhuman primate. Male Macaca fascicularis monkeys underwent chronic bilateral renal denervation or sham surgery. After a 1- to 2-wk recovery period, each animal was anesthetized with pentobarbital sodium and volume expanded 20% of estimated blood volume. Two types of volume expansion were used, a hemodilutional expansion using 6% dextran in isotonic saline and an isohemic expansion using each monkey's own blood that had previously been withdrawn in exchange for dextran. Renal denervation did not attenuate the excretory responses to volume expansion in that similar increases in urine flow, sodium excretion, filtered load of sodium excreted, osmolar and free water clearances occurred in both the renal-denervated and sham-operated groups. The onset of the responses was not delayed by renal denervation. Furthermore, the results were the same with both volume expansions. These results suggest that, in the monkey, decreases in renal nerve activity that occur with volume expansion are not necessary for eliciting the excretory responses to this hypervolemic stimulus or that other factors compensate if the kidneys are chronically denervated. In addition, the failure of renal denervation to attenuate the excretory effects of a cell-free volume expansion is not related to any dilutional characteristics of the expansion.

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