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)

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.

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.

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)

Saline diuresis and natriuresis in unanesthetized dogs: a missing atrial factor?

1992 ◽  
Vol 263 (3) ◽  
pp. H792-H797
Author(s):  
A. W. Cowley ◽  
A. G. Brice ◽  
M. M. Skelton
Keyword(s):  
Plasma Renin ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Cardiac Denervation ◽  
Volume Load ◽  
Before And After ◽  
Intravenous Saline ◽  
Renal Nerve Activity ◽  
The Central Nervous System

Recent studies in our laboratory indicated that a blunted (40–50%) renal excretory response to isotonic intravenous saline loads occurred in conscious, renal-denervated dogs after 70% of the atrial mass was removed. The blunted responses could not be explained by differences in the responses of arterial pressure, renal nerve activity, or by measured changes of plasma immunoreactive atrial natriuretic peptide (iANP), arginine vasopressin (AVP), plasma renin activity (PRA), or aldosterone (Aldo). The present study was designed to determine whether the central nervous system (CNS) was the source of an unidentified substance, which could account for the blunting of the urine excretory response seen in the atrial-resected dogs. Renal denervation was performed in all dogs to eliminate alterations in efferent renal sympathetic nerve activity derived from reflexes activated during volume expansion. Cardiac denervation (CDX) was used to eliminate sensory cardiac afferent nerve activity to the CNS. A group of five renal-denervated dogs was given an isotonic volume load (400 ml/30 min) before and after complete CDX. Plasma AVP was fixed at normal plasma levels of 3 pg/ml by continuous intravenous infusion. Na and H2O excretion were not different in renal-denervated dogs compared with combined renal and cardiac denervation during the 5 h after the saline load. Plasma AVP and Aldo were unchanged with the volume loads, although PRA rose gradually over the 5 h after the saline loads. Plasma iANP increased transiently in the combined renal and cardiac-denervated state rising from a control of 65–120 pg/ml at the end of the load period.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

Effect of sympathetic sensitization of baroreceptors on renal nerve activity

1987 ◽  
Vol 252 (2) ◽  
pp. R328-R335 ◽  
Author(s):  
J. L. Seagard ◽  
F. A. Hopp ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Activity ◽  
Carotid Sinus ◽  
Baroreceptor Sensitivity ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Before And After ◽  
Renal Nerve Activity ◽  
Sinus Pressure ◽  
Renal Sympathetic

The role of sympathetic efferent innervation of the carotid sinus on the regulation of baroreceptor sensitivity was examined in thiopental-sodium anesthetized dogs (5 mg X kg-1 X h-1 infusion). Baroreflex sensitivity was defined as the slope of renal sympathetic efferent nerve activity vs. carotid sinus pressure in an isolated, perfused carotid sinus. Slopes were obtained before and after sinus sympathectomy performed by section of the cervical sympathetic trunk. There was no significant differences between baroreflex decreases in renal sympathetic activity due to increases in carotid sinus pressure before and after sympathectomy, but the responses to decreases in carotid sinus pressure after sympathectomy were significantly greater than control. Base-line level of renal sympathetic activity, obtained at a constant perfusion pressure of 115 mmHg, abruptly increased by 11% in response to sinus sympathectomy. The response of baroreceptors to sympathomimetic stimulation was examined by recording carotid baroreceptor afferent nerve activity during ramp changes in carotid sinus pressure after addition of epinephrine (10(-8) to 10(-6) M) to the perfusate of the sympathetically denervated sinus. The slopes of the sinus nerve activity vs. carotid sinus pressure were used as direct indexes of baroreceptor sensitivity. Lower levels of epinephrine (10(-8), 10(-7) M) increased the sensitivity of the baroreceptors and reduced renal nerve activity back toward presympathectomy levels. A higher dose of epinephrine (10(-6) M) did not significantly increase baroreceptor sensitivity. The results of this study suggest that sinus sympathetic fibers produce a tonic sensitization of the baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Renorenal reflexes: Interaction between efferent and afferent renal nerve activity

1992 ◽  
Vol 70 (5) ◽  
pp. 750-758 ◽  
Author(s):  
Ulla C. Kopp
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Vena Cava ◽  
Reflex Response ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Central Interaction ◽  
Renal Nerve Activity

In rats, stimulation of renal mechanoreceptors by increasing ureteral pressure results in a contralateral inhibitory renorenal reflex response consisting of increases in ipsilateral afferent renal nerve activity, decreases in contralateral efferent renal nerve activity, and increases in contralateral urine flow rate and urinary sodium excretion. Mean arterial pressure is unchanged. To study possible functional central interaction among the afferent renal nerves and the aortic and carotid sinus nerves, the responses to renal mechanoreceptor stimulation were compared in sinoaortic denervated rats and sham-denervated rats before and after vagotomy. In contrast to sham-denervated rats, there was an increase in mean arterial pressure in response to renal mechanoreceptor stimulation in sinoaortic-denervated rats. However, there were no differences in the renorenal reflex responses among the groups. Thus, our data failed to support a functional central interaction among the renal, carotid sinus, and aortic afferent nerves in the renorenal reflex response to renal mechanoreceptor stimulation. Studies to examine peripheral interaction between efferent and afferent renal nerves showed that marked reduction in efferent renal nerve activity produced by spinal cord section at T6, ganglionic blockade, volume expansion, or stretch of the junction of superior vena cava and right atrium abolished the responses in afferent renal nerve activity and contralateral renal function to renal mechanoreceptor stimulation. Conversely, increases in efferent renal nerve activity caused by thermal cutaneous stimulation increased basal afferent renal nerve activity and its responses to renal mechanoreceptor stimulation. These data suggest a facilitatory role of efferent renal nerves on renal sensory receptors.Key words: vagotomy, sinoaortic denervation, substance P, prostaglandins, mechanoreceptor stimulation.

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