Renal nerve activity in conscious rats during volume expansion and depletion

1985 ◽  
Vol 248 (1) ◽  
pp. F15-F23 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin

The role of renal nerve activity (RNA) in the renal response to isotonic saline volume expansion and furosemide-induced volume depletion was studied in conscious rats consuming a low (LNa), normal (NNa), or high (HNa) dietary sodium intake. In the control state, right atrial pressure (RAP) and UNa V were directly related and RNA was inversely related to dietary sodium intake, being 12.9 +/- 0.7, 10.9 +/- 1.1 and 8.7 +/- 0.6 units in LNa, NNa, and HNa rats, respectively. During volume expansion, RAP and UNa V increased and RNA decreased in all three dietary groups; however, the peak increase in UNa V was greater in the LNa (88 +/- 6 mueq/min) than NNa (34 +/- 9 mueq/min) or HNa (32 +/- 6 mueq/min) rats. The greater natriuresis in LNa was associated with a larger decrease in RNA in LNa (-6.1 +/- 0.5 units) than in NNa (-3.4 +/- 0.4 units). The greater contribution of inhibition of RNA to the increased natriuretic response to volume expansion in LNa compared with NNa rats was further examined in renal denervated animals. Bilateral renal denervation substantially reduced the natriuretic response to volume expansion in LNa rats (-70%) but had no significant effect in NNa rats (-15%). During volume depletion, RAP decreased, whereas UNa V and RNA increased in all three dietary groups. After the peak of the furosemide natriuresis, UNa V was lower in the LNa rats than in the NNa or HNa rats at any level of increased RNA, consistent with a role for the renal nerves in the normal renal adaptive response to sodium/volume depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

1977 ◽  
Vol 233 (5) ◽  
pp. H592-H599 ◽  
Author(s):  
L. C. Weaver

Cardiopulmonary sympathetic afferent nerves may affect renal control of intravascular volume by influencing renal sympathetic nerve activity. This influence was evaluated in alpha-chloralose anesthetized, vagotomized, sino-aortic denervated cats. When the afferent nerves were activated with a single electrical stimulus, the renal nerve responded with an excitatory burst of activity followed by a long period of inhibition. This response had characteristics of a supraspinal reflex. Repetitive stimulation of the sympathetic afferent nerve either inhibited or excited renal nerves and increased or decreased systemic blood pressure. The direction of these changes depended on stimulus parameters. No obligatory correlation in the direction of change of nerve activity and blood pressure was observed. Activation of cardiopulmonary sympathetic afferent nerves by intravascular volume expansion inhibited renal nerve discharge. Inhibition was elminated by sectioning the sympathetic afferent nerves. Volume expansion had no effect on lumbar sympathetic discharge monitored simultaneously with renal nerve activity. This observation suggests specificity of reflex influences of these afferent nerves on the kidney. In conclusion, cardiopulmonary sympathetic afferent nerves can reflexly alter renal nerve activity, and therefore may affect renal control of intravascular volume.


1992 ◽  
Vol 70 (5) ◽  
pp. 733-734 ◽  
Author(s):  
J. Michael Wyss

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.


1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath

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.


1996 ◽  
Vol 271 (6) ◽  
pp. R1489-R1499 ◽  
Author(s):  
S. C. Malpas ◽  
A. Shweta ◽  
W. P. Anderson ◽  
G. A. Head

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.


1982 ◽  
Vol 242 (6) ◽  
pp. F592-F598 ◽  
Author(s):  
J. P. Gilmore ◽  
S. Echtenkamp ◽  
C. R. Wesley ◽  
I. H. Zucker

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.


1992 ◽  
Vol 262 (5) ◽  
pp. R834-R841 ◽  
Author(s):  
N. G. Moss ◽  
A. B. Scoltock

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)


1988 ◽  
Vol 254 (1) ◽  
pp. F32-F37 ◽  
Author(s):  
G. Szenasi ◽  
G. Kottra ◽  
P. Bencsath ◽  
L. Takacs

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)


1983 ◽  
Vol 244 (1) ◽  
pp. F64-F69 ◽  
Author(s):  
C. R. Silva-Netto ◽  
R. H. Jackson ◽  
R. E. Colindres

We investigated possible mechanisms for the natriuresis seen after injection of the cholinergic drug carbamylcholine chloride (carbachol) into the lateral hypothalamus of conscious rats. In unrestrained rats injection of 1 microgram of carbachol in 1 microliter of 0.15 M NaCl solution through a permanently implanted cannula produced a significant natriuresis and kaliuresis. Injection of vehicle produced no changes. The same animals were then subjected to bilateral renal denervation (n = 13) or sham denervation (n = 13) and injected with the same solutions 1 wk later. Carbachol injection produced a natriuresis (P less than 0.0001) and a kaliuresis (P less than 0.01) in all animals studied. Both responses were of a magnitude similar to the responses seen before denervation. We studied other rats while awake but restrained, which permitted the performance of clearance studies and blood pressure measurements. Injection of carbachol produced diuresis, natriuresis, and kaliuresis in all rats, with no change in p-aminohippurate clearance and only transient change in inulin clearance. An increase in blood pressure occurred in some but not all rats. The response in rats with bilaterally denervated kidneys (n = 7) was similar to that of rats with innervated kidneys (n = 5). The natriuresis seen after cholinergic stimulation of the hypothalamus in conscious rats is not primarily mediated by inhibition of renal nerve activity and can be dissociated from changes in blood pressure, glomerular filtration rate, and renal plasma flow.


1990 ◽  
Vol 68 (4) ◽  
pp. 524-530 ◽  
Author(s):  
P. F. Mercer ◽  
R. L. Kline

The role of the renal nerves in the electrolyte excretion of rats fed or fasted overnight was determined in conscious rats and anesthetized (Inactin) and surgically prepared rats. In conscious rats sodium excretion, as measured in a 1-h urine collection period after feeding or fasting overnight, was decreased with fasting with or without renal nerves. Renal nerve activity, as measured by norepinephrine turnover (inhibition of tyrosine hydroxylase by α-methyl-p-tyrosine), was not different between conscious fed or fasted rats and increased to the same extent in fed and fasted rats when anesthetized and surgically prepared. Anesthetized, surgically prepared rats infused with 5.0% glucose showed a denervation natriuresis if rats were fed overnight, but not if they had been fasted overnight. Potassium excretion in conscious and anesthetized rats was lower in fasted rats than fed rats with or without renal nerves. These data suggest (i) renal nerves are not involved in the renal response to an overnight fast in conscious rats, and (ii) in anesthetized, surgically prepared rats renal sympathetic tone is enhanced and denervation natriuresis occurs if rats are fed but not if fasted. Potassium excretion is a reflection of whether rats are fed or fasted and not whether they have renal nerves.Key words: kidney, fasting, sodium, renal nerves.


1976 ◽  
Vol 51 (1) ◽  
pp. 93-102 ◽  
Author(s):  
E. J. Johns ◽  
Barbara A. Lewis ◽  
Bertha Singer

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.


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