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.

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.

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.

Neurogenic regulation of proximal bicarbonate and chloride reabsorption

1986 ◽  
Vol 250 (1) ◽  
pp. F22-F26 ◽  
Author(s):  
M. G. Cogan
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sprague Dawley ◽  
Electrolyte Excretion ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Single Nephron ◽  
Renal Nerve Activity ◽  
Chloride Excretion

Although a change in renal nerve activity is known to alter proximal reabsorption, it is unclear whether reabsorption of NaHCO3 or NaCl or both are affected. Sprague-Dawley rats (n = 10) were studied using free-flow micropuncture techniques during euvolemia and following acute ipsilateral denervation. Glomerular filtration rate and single nephron glomerular filtration rate were stable. Absolute proximal bicarbonate reabsorption fell following denervation (933 +/- 40 to 817 +/- 30 pmol/min) with a parallel reduction in chloride reabsorption (1,643 +/- 116 to 1,341 +/- 129 peq/min). Urinary sodium, potassium, bicarbonate, and chloride excretion all increased significantly. To further assess the physiological significance of neurogenic modulation of proximal transport, other rats (n = 6) were subjected to acute unilateral nephrectomy (AUN). There is evidence that AUN induces a contralateral natriuresis (renorenal reflex) at least partially by causing inhibition of efferent renal nerve traffic. AUN caused significant changes in proximal NaHCO3 and NaCl reabsorption as well as in whole kidney electrolyte excretion in the same pattern as had denervation. Prior denervation of the remaining kidney prevented the proximal and whole kidney response to AUN (n = 6). In conclusion, depression of renal nerve activity inhibits both NaHCO3 and NaCl reabsorption in the rat superficial proximal convoluted tubule. The data are consistent with the hypothesis that changes in renal nerve activity modify whole kidney electrolyte excretion under physiological conditions at least partially by regulating proximal transport.

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.

Renal function and renal afferent and efferent nerve activity

1982 ◽  
Vol 243 (5) ◽  
pp. F425-F433 ◽  
Author(s):  
N. G. Moss
Keyword(s):  
Renal Function ◽  
Direct Action ◽  
Renal Nerves ◽  
Renal Tubules ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Efferent Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity ◽  
Stimulation Of

Recent microperfusion studies have fully substantiated the direct action of catecholamines on renal tubular reabsorptive rates. Surprisingly, these techniques have not provided consistent information on the nature of the adrenoceptor responsible for the stimulation of proximal tubular reabsorption. Both alpha- and beta-receptors have been favored for this role. These techniques have confirmed earlier reports that dopamine may have a direct natriuretic action on the renal tubules. The demonstration that renal efferent nerves contain both noradrenergic and dopaminergic fibers lends further support for the participation of dopamine in the regulation of salt and water excretion. Efferent renal nerve activity is modulated by a number of different afferent inputs to the central nervous system. One of these is the renal afferent innervation, which is composed of both chemoreceptor and mechanoreceptor fibers. A number of different reflexes that affect efferent renal nerve activity have been identified by electrical stimulation of renal afferent nerves or by selective stimulation of renal mechanoreceptors and chemoreceptors. These renorenal reflexes may have importance in the coordination of excretory activity between the two kidneys. Studies of these aspects of renal nerve function are reviewed. The importance of the renal nerves in conscious animals is also discussed in the light of evidence that their influence on renal function may be more apparent in abnormal or pathological circumstances.

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.

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.

Atrial receptor modulation of renal nerve activity in the nonhuman primate

1982 ◽  
Vol 242 (6) ◽  
pp. F592-F598 ◽  
Author(s):  
J. P. Gilmore ◽  
S. Echtenkamp ◽  
C. R. Wesley ◽  
I. H. Zucker
Keyword(s):  
Significant Influence ◽  
Nonhuman Primate ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Balloon Inflation ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Receptor Modulation ◽  
Renal Nerve Activity ◽  
Cervical Vagotomy

Experiments were done in the nonhuman primate Macaca fascicularis to determine the extent to which low-pressure receptors modulate renal nerve activity (RNA). Left atrial pressure (LAP) was increased either by inflating a balloon in the left atrium or by intravascular volume expansion. Arterial pressure (AP) was increased by the administration of epinephrine. Balloon inflation produced variable changes in RNA when all reflexes were intact. In the bilateral vagotomized animal, balloon inflation significantly increased RNA. Compared with the intact state, neither carotid sinus denervation nor sinoaortic denervation had a significant influence on RNA during balloon inflation. The response of both baroreceptor-denervated groups, however, was significantly less than that of the vagotomized group. Vagotomy plus sinoaortic denervation essentially prevented any effect of balloon inflation on RNA. Volume expansion produced a greater inhibition of RNA per increase in AP than did epinephrine. However, this difference was abolished after bilateral cervical vagotomy. These experiments demonstrate a significant influence and interplay of low- and high-pressure receptors on RNA in the nonhuman primate.

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