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

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.

1982 ◽  
Vol 63 (s8) ◽  
pp. 215s-217s ◽  
Author(s):  
R. Golin ◽  
A. Stella ◽  
A. Zanchetti

1. In anaesthetized cats, reversible nenal nerve denervation (cooling of the renal nerves on one side at 4°C for 16 min) was performed and its effects on haemodynamic and excretory functions of the ipsilateral and the contralateral kidneys were studied. 2. Renal nerve cooling did not cause any change in arterial pressure. Slight increase in blood flow, no change in glomerular filtration rate and a large increase in water and sodium excretion occurred in the ipsilateral kidney; simultaneously, no change in blood flow, a slight and transient decrease in glomerular filtration rate, and a significant decrease in diuresis and natriuresis were observed in the contralateral kidney. 3. Ipsilateral and contralateral renal changes were equally evident in the early (minutes 0 to 8) and late phases (minutes 8 to 16) of the cooling period. 4. When renal nerve cooling was repeated after surgical denervation of the contralateral kidney all contralateral effects were abolished.


1986 ◽  
Vol 250 (1) ◽  
pp. F22-F26 ◽  
Author(s):  
M. G. Cogan

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.


1983 ◽  
Vol 245 (6) ◽  
pp. F763-F771 ◽  
Author(s):  
D. Beasley ◽  
R. L. Malvin ◽  
D. R. Mouw

Sodium excretion was studied following experimental elevation of cerebrospinal fluid (CSF) sodium in heterozygous and homozygous (DI) Brattleboro rats given exogeneous antidiuretic hormone. Sodium excretion increased 4.5-fold in heterozygous and 3.5-fold in DI rats. The natriuresis in both groups was rapid in onset and occurred with a simultaneous kaliuresis. Blood pressure increased approximately 10 mmHg in the heterozygous but not in the DI rats. Accordingly, increased blood pressure may contribute to the natriuresis but is not the sole mechanism. Plasma renin concentration did not change in the DI rats during high Na CSF infusion, and chronic bilateral renal denervation did not abolish the natriuresis. Glomerular filtration rate increased during the high Na period in both the intact and renally denervated rats. These data provide evidence that a natriuretic mechanism exists that is not mediated by changes in antidiuretic hormone, renal nerve activity, mean arterial pressure, aldosterone, or angiotensin II, and thus may be due to another circulating substance or natriuretic hormone. This hormone may act totally or in part by increasing glomerular filtration rate.


1982 ◽  
Vol 93 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Stephen Ball ◽  
E. J. Johns

The renal nerves of the left kidney of sodium-replete anaesthetized rats were stimulated for 30-min periods at 2–3 Hz (15 V, 0·2 ms). Renal blood flow was reduced by 22% and glomerular filtration rate by 14% which resulted in a rise in filtration fraction of 12%. Circulating plasma renin activity was increased by 30% during such nerve stimulation. In rats treated for 3–4 weeks with deoxycorticosterone acetate (DOCA) and saline (150 mm-NaCl) basal values of arterial blood pressure, renal blood flow, glomerular filtration rate and filtration fraction were not significantly different from those observed in sodium-replete rats. However, plasma renin activity was lower, being approximately one-third of that observed in sodium-replete animals. Stimulation of the renal nerves in rats treated with DOCA and saline resulted in a fall in renal blood flow of 32% and a much larger fall in glomerular filtration rate of 33% which resulted in no change in filtration fraction. Plasma renin activity was not changed by renal nerve stimulation in the animals treated with DOCA and saline. It is suggested that these renal responses provide evidence in the rat for a role of locally generated angiotensin II in regulating glomerular filtration rate during electrical activation of the renal nerves by causing preferential vasoconstriction of the efferent arteriole.


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.


1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.


1989 ◽  
Vol 257 (6) ◽  
pp. R1519-R1525 ◽  
Author(s):  
F. G. Smith ◽  
T. Sato ◽  
O. J. McWeeny ◽  
L. Torres ◽  
J. E. Robillard

The present study was designed to determine the influence of renal nerves in mediating the renal response to volume expansion in conscious newborn lambs. Bilateral renal denervation (n = 9) or sham surgery (n = 14) was carried out in newborn lambs 3 to 4 days before performing experiments. Lambs were between 6 and 12 days of age when studied. Chronic denervation did not alter basal neonatal renal function nor renal hemodynamics. Volume expansion with isotonic saline equal to 5% of body weight was associated with a fall in hematocrit and an increase in mean arterial blood pressure, glomerular filtration rate, urine flow rate, and Na+ excretion in intact and denervated lambs. In intact lambs, atrial natriuretic factor increased from 98 +/- 28 to 176 +/- 48 ng/ml during volume expansion and remained elevated for 1 h after volume expansion. In addition, plasma renin activity fell from 21 +/- 5 to 8 +/- 1 ng.ml-1.h-1 and aldosterone levels fell from 160 +/- 24 to 59 +/- 7 pg/ml by 150 min after the start of volume expansion. Similar changes in atrial natriuretic factor, plasma renin activity, and aldosterone were observed in denervated lambs. However, the increase in glomerular filtration rate, Na+ excretion, and fractional excretion of Na+ after volume expansion were significantly less in denervated than in intact lambs. Thus, in the newborn, the renal nerves do not appear to play a role in influencing basal renal hemodynamics and renal function but, as in the adult, the renal sympathetic nervous system does play a role in regulating fluid and electrolyte excretion during hypervolemia.


1979 ◽  
Vol 56 (4) ◽  
pp. 365-371 ◽  
Author(s):  
E. J. Johns

1. The renal responses to low level renal nerve stimulation and reduction in renal perfusion pressure within the autoregulatory range were measured before and after blockade of converting enzyme activity. Experiments were carried out using the unilaterally nephrectomized cat with the nerves of the remaining kidney acutely sectioned. 2. Renal nerves were stimulated to cause a 14% fall in blood flow for 15 min. Glomerular filtration rate was unchanged but sodium excretion and the ratio of sodium clearance to glomerular filtration rate fell significantly. 3. Renal nerve stimulation after blockade of converting enzyme activity was associated with a significant fall in glomerular filtration rate. The reductions in sodium excretion and in the ratio of sodium clearance to glomerular filtration rate were as large as in the absence of the blocking drug. 4. Reduction in renal perfusion pressure was associated with autoregulation of both renal blood flow and glomerular filtration rate but with large falls in sodium excretion and the ratio of sodium clearance to glomerular filtration rate. 5. After blockade of converting enzyme activity blood flow was still autoregulated in response to similar perfusion pressure reduction and glomerular filtration rate fell significantly. The ratio of sodium clearance to glomerular filtration rate, and sodium excretion, were reduced to the same extent as in the absence of the drug. 6. This information suggests that regulation of glomerular filtration rate associated with nerve stimulation or pressure reduction may be mediated by the intrarenal formation of angiotensin II, possibly acting at the efferent arteriole. They also indicate that angiotensin II is probably not involved in causing the increased sodium reabsorption.


1982 ◽  
Vol 62 (5) ◽  
pp. 457-464 ◽  
Author(s):  
A. T. Veressa ◽  
C. K. Chong ◽  
H. Sonnenberg

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.


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