Renal nerves in compensatory renal response to contralateral renal denervation

1980 ◽  
Vol 238 (1) ◽  
pp. F26-F30 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Rios
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Left Kidney ◽  
Fractional Excretion ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Renal Response ◽  
Fractional Sodium Excretion ◽  
Fractional Excretion Of Sodium ◽  
Renal Sympathetic

Acute unilateral renal denervation and the resultant antidiuresis and antinatriuresis are accompanied by a compensatory antidiuresis and antinatriuresis from the opposite kidney. The present study tested the hypothesis that the renal sympathetic nerves mediated this adaptive response. In the volume-expanded rat, acute left renal denervation increased left kidney fractional sodium excretion from 4.4 +/- 0.6 to 5.9 +/- 0.6%, while right kidney fractional sodium excretion decreased from 4.3 +/- 0.6 to 3.5 +/- 0.5%. Subsequent acute right renal denervation increased right kidney fractional sodium excretion from 3.5 +/- 0.5 to 4.7 +/- 0.6%. Measurement of efferent left renal sympathetic nerve activity before and after acute right renal denervation showed an increase from 10.9 +/- 0.8 to 16.0 +/- 1.4 Hz. When both kidneys were simultaneously subjected to acute renal denervation, fractional excretion of sodium increased bilaterally. In uninephrectomized rats subjected to acute denervation of the remaining kidney, fractional excretion of sodium increased. Glomerular filtration rate was unchanged throughout in all studies. These results demonstrate that the compensatory renal response to acute contralateral renal denervation is mediated by the efferent renal sympathetic nerves.

Antagonistic effect of theophylline on the adenosine-induced decreased in renin release

1984 ◽  
Vol 247 (2) ◽  
pp. F246-F251 ◽  
Author(s):  
W. S. Spielman
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Renal Cortex ◽  
Fractional Excretion ◽  
Antagonistic Effect ◽  
Renin Release ◽  
Detectable Effect ◽  
Fractional Sodium Excretion ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs

The action of theophylline on the adenosine-induced decrease in renin release was studied in anesthetized dogs. Adenosine inhibited renin release, decreased GFR and fractional sodium excretion, and decreased the concentration of angiotensin II in the renal lymph. Theophylline (5 mumol/min intrarenally) had no significant effect on GFR or RBF yet produced a significant increase in the release of renin and the fractional excretion of sodium. The intrarenal infusion of adenosine (3 X 10(-7) mol/min) during theophylline infusion produced no effect on GFR or RBF, but fractional sodium excretion and renin release were significantly decreased. Adenosine was infused at a lower dose (3 X 10(-8) mol/min) during theophylline (5 X 10(-6) mol/min) infusion in a second group of dogs. With the exception of fractional sodium excretion, all effects of adenosine were effectively antagonized by theophylline. Theophylline at 5 X 10(-6) mol/min, which stimulates renin release and effectively antagonizes the renal effects of adenosine, had no detectable effect on cAMP measured in renal cortex. Furthermore, no change in cortical cAMP was observed until theophylline was increased 50-fold over the dose effective in antagonizing adenosine. These findings demonstrate that theophylline, at concentrations having no effect on cortical cAMP, antagonizes the effect of adenosine on renin release. The results are also consistent with the view that theophylline stimulates renin release by a mechanism other than its action on cAMP.

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs

1998 ◽  
Vol 275 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
Francine G. Smith ◽  
Isam Abu-Amarah
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Elevated Plasma ◽  
Baseline Levels ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 ± 16 to 207 ± 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 ± 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 ± 6.4 ng ANG I ⋅ ml−1 ⋅ h−1) compared with intact lambs (4.0 ± 1.1 ng ANG I ⋅ ml−1 ⋅ h−1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 ± 8 to 197 ± 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 ± 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

Role of renal nerves in natriuresis of L-NMMA infusion in SHR and WKY rats

1995 ◽  
Vol 269 (1) ◽  
pp. F17-F21 ◽  
Author(s):  
A. A. Khraibi
Keyword(s):  
Renal Denervation ◽  
Spontaneously Hypertensive Rat ◽  
Left Kidney ◽  
Acute Experiment ◽  
Renal Nerves ◽  
High Dose ◽  
Wky Rats ◽  
Fractional Excretion Of Sodium ◽  
Shr And Wky Rats

The purpose of this study was to determine the role of the renal nerves in the natriuresis and diuresis that is observed with the systemic infusion of a high dose of NG-monomethyl-L-arginine (L-NMMA) to inhibit nitric oxide synthesis in the Okamoto spontaneously hypertensive rat (SHR) and the Wistar-Kyoto (WKY) rat. All rats in this study underwent a unilateral nephrectomy approximately 2 wk prior to the acute experiment. On the day of the acute experiment, renal denervation of the remaining left kidney was performed in one group of SHR (n = 6) and one group of WKY rats (n = 9). Another group of SHR (n = 6) and WKY rats (n = 10) had an innervated kidney. A control clearance period was taken, and then an L-NMMA (15 mg/kg bolus followed by 500 micrograms.kg-1.min-1 continuous infusion) infusion period followed in all four groups of rats. In the innervated SHR and WKY rats, the increases in fractional excretion of sodium (FENa) were 5.11 +/- 0.70 and 3.58 +/- 0.38%, respectively, with the infusion of L-NMMA and were associated with significant increases in fractional excretions of phosphate (FEPi; 18.18 +/- 5.33 and 6.34 +/- 2.29%, respectively), suggesting a reduction in proximal tubule reabsorption. In the SHRs with acute renal denervation, FENa was significantly increased by L-NMMA; however, FENa was significantly reduced (2.03 +/- 0.70%; P < 0.05) in comparison with innervated SHRs and was associated with no increase in FEPi (FEPi = -0.72 +/- 1.23%).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Interactions between nitric oxide and renal nerves on pressure-diuresis and natriuresis.

1998 ◽  
Vol 9 (9) ◽  
pp. 1588-1595
Author(s):  
M I Madrid ◽  
M G Salom ◽  
J Tornel ◽  
E López ◽  
F J Fenoy
Keyword(s):  
Nitric Oxide ◽  
Renal Denervation ◽  
Fractional Excretion ◽  
Renal Nerves ◽  
High Dose ◽  
Lower Baseline ◽  
Fractional Excretion Of Sodium ◽  
Natriuretic Effect ◽  
High Doses ◽  
Pressure Natriuresis

The present study examined the effect of renal denervation on the impairment of the pressure-diuresis response produced by nitric oxide synthesis blockade. The experiments were performed in Inactin-anesthetized Munich-Wistar rats. The animals with innervated kidneys had lower baseline values of renal blood flow, GFR, sodium excretion (UNaV), and urine flow (V) than rats with denervated kidneys. Also, renal denervation shifted pressure-diuresis and natriuresis toward lower pressures. A low dose of N(omega)-nitro-L-arginine methyl esther (NAME, 3.7 nmol/kg per min) reduced UNaV and the fractional excretion of sodium (FENa) and blunted pressure-natriuresis only in rats with innervated kidneys, whereas it had no effects in rats with denervated kidneys. A medium dose of NAME (37 nmol/kg per min) lowered FENa only in rats with innervated kidneys. The administration of NAME (37 nmol/kg per min) blunted pressure-diuresis and natriuresis in kidneys with or without the renal nerves, but the effect was more pronounced in rats with innervated kidneys. A high dose of NAME (3.7 micromol + 185 nmol/kg per min) increased UNaV and FENa only in rats with innervated kidneys, whereas it reduced GFR, V, UnaV, and FENa in rats with denervated kidneys. However, pressure-natriuresis and diuresis were blunted by this high dose of NAME independently of the presence or absence of renal nerves. These results demonstrate that renal nerves potentiate the renal effects of low doses of NAME on renal function and pressure-diuresis and natriuresis. However, high doses of NAME abolish pressure-diuresis independently of renal nerves, and the natriuretic effect of NAME in innervated kidneys may be attributed to reflex inhibition of sympathetic tone due to the rise in arterial pressure.

Effects of renal denervation on cardiovascular response to furosemide in conscious lambs

1995 ◽  
Vol 269 (1) ◽  
pp. H149-H152 ◽  
Author(s):  
F. G. Smith ◽  
A. M. Strack
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Renal Denervation ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Before And After ◽  
Renal Sympathetic

The cardiovascular response to furosemide in the newborn and the role of renal sympathetic nerves in influencing this response have not been investigated. We hypothesized that in conscious lambs, furosemide would decrease blood pressure, the response being accentuated in the absence of renal sympathetic nerves. Pulsatile pressures and heart rates were measured before and after furosemide (2 mg/kg) administration to chronically instrumented lambs with either bilateral renal denervation (denervated, n = 8) or renal nerves intact (intact, n = 6). In intact lambs, mean arterial pressure remained constant after furosemide; in denervated lambs there was an increase in arterial pressure 20 min after furosemide (P < 0.001), and control levels were reached by 100 min. Basal heart rate was higher in denervated than in intact lambs (P = 0.009). In both groups of lambs, heart rate increased 40 min after furosemide and remained elevated. These data provide new information that, in conscious newborn animals, renal sympathetic nerves influence the blood pressure response to furosemide, as well as basal control of heart rate.

Altered responsiveness of the kidney to activation of the renal nerves in fat-fed rabbits

2009 ◽  
Vol 296 (6) ◽  
pp. R1889-R1896 ◽  
Author(s):  
Sylvia Michaels ◽  
Gabriela A. Eppel ◽  
Sandra L. Burke ◽  
Geoffrey A. Head ◽  
James Armitage ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Neural Control ◽  
Control Diet ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Urine Flow ◽  
Renal Nerves ◽  
Renal Nerve ◽  
And Control ◽  
Renal Sympathetic

We tested whether mild adiposity alters responsiveness of the kidney to activation of the renal sympathetic nerves. After rabbits were fed a high-fat or control diet for 9 wk, responses to reflex activation of renal sympathetic nerve activity (RSNA) with hypoxia and electrical stimulation of the renal nerves (RNS) were examined under pentobarbital anesthesia. Fat pad mass and body weight were, respectively, 74% and 6% greater in fat-fed rabbits than controls. RNS produced frequency-dependent reductions in renal blood flow, cortical and medullary perfusion, glomerular filtration rate, urine flow, and sodium excretion and increased renal plasma renin activity (PRA) overflow. Responses of sodium excretion and medullary perfusion were significantly enhanced by fat feeding. For example, 1 Hz RNS reduced sodium excretion by 79 ± 4% in fat-fed rabbits and 46 ± 13% in controls. RNS (2 Hz) reduced medullary perfusion by 38 ± 11% in fat-fed rabbits and 9 ± 4% in controls. Hypoxia doubled RSNA, increased renal PRA overflow and medullary perfusion, and reduced urine flow and sodium excretion, without significantly altering mean arterial pressure (MAP) or cortical perfusion. These effects were indistinguishable in fat-fed and control rabbits. Neither MAP nor PRA were significantly greater in conscious fat-fed than control rabbits. These observations suggest that mild excess adiposity can augment the antinatriuretic response to renal nerve activation by RNS, possibly through altered neural control of medullary perfusion. Thus, sodium retention in obesity might be driven not only by increased RSNA, but also by increased responsiveness of the kidney to RSNA.

Renal nerves and renal responses to head-up tilt in dogs

1987 ◽  
Vol 252 (5) ◽  
pp. R979-R986
Author(s):  
T. V. Peterson ◽  
N. L. Hurst ◽  
J. A. Richardson
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Urine Flow ◽  
Renal Nerves ◽  
Fluid Reabsorption ◽  
Fractional Sodium Excretion ◽  
Head Up Tilt ◽  
Anesthetized Dogs ◽  
Renal Responses

Experiments were performed in anesthetized dogs to compare the effects of acute and chronic unilateral renal denervation on the renal responses to head-up tilt and to assess denervation hypersensitivity to infused norepinephrine (NE). Responses of the denervated kidney were compared with those of the contralateral innervated kidney in each animal. With acute denervation, 40 min of 45 degrees head-up tilt decreased urine flow (V) 37%, absolute sodium excretion (UNaV) 53%, and fractional sodium excretion (FENa+) 44% in the innervated kidneys, but no decreases occurred in the denervated kidneys. NE infusion (125 ng X kg-1 X min-1) increased arterial pressure by 11 mmHg and increased V, UNaV, and FENa+ in both kidneys. In the chronically denervated animals (2-4 wk prior to experiment) tilt decreased V by 32%, UNaV by 44%, and FENa+ by 21% in the innervated kidneys, but again no changes occurred in the denervated kidneys. NE infusion in this group also increased arterial pressure approximately 11 mmHg and caused V, UNaV, and FENa+ to increase in the innervated kidneys but decrease in the denervated kidneys. These results demonstrate that the renal responses to tilt are abolished by both acute and chronic renal denervation even though the chronically denervated kidney is hypersensitive to NE-stimulated fluid reabsorption. Therefore endogenous plasma NE levels must not increase enough during tilt such that this hypersensitivity phenomenon can compensate for chronic ablation of the renal nerves.

Pentobarbital anesthesia alters renal actions of alpha-hANP in dogs

1990 ◽  
Vol 258 (3) ◽  
pp. R616-R623 ◽  
Author(s):  
J. B. Madwed ◽  
B. C. Wang
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Control Period ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Renal Responses ◽  
Renal Sympathetic

The magnitude of the natriuretic response to an infusion of alpha-human atrial natriuretic peptide (alpha-hANP) has varied considerably in different studies. The greatest renal responses to alpha-hANP infusion have been observed in barbiturate-anesthetized dogs. We therefore examined the renal, hormonal, and cardiovascular responses to alpha-hANP infusion in eight female dogs, once awake and again anesthetized with pentobarbital sodium (25 mg/kg body wt). After a 20-min control period, alpha-hANP was infused at a rate of 25 ng.kg-1.min-1 for 60 min. In dogs when awake, infusion of alpha-hANP produced a significant increase in sodium excretion from a control value of 39 +/- 7 to 73 +/- 13 and 89 +/- 15 mu eq/min after 40 and 60 min. In dogs when anesthetized, infusion of alpha-hANP produced an increase in sodium excretion from 21 +/- 3 to 105 +/- 12 and 143 +/- 21 mu eq/min after 40 and 60 min. The increase in sodium excretion was significantly greater in dogs when anesthetized than when awake. We also investigated the role of the renal sympathetic nerves on these responses in six dogs after chronic bilateral renal denervation. In dogs with denervated kidneys when awake, infusion of alpha-hANP did not change sodium excretion significantly. In dogs with denervated kidneys when anesthetized, infusion of alpha-hANP significantly increased sodium excretion; however, the increase was significantly attenuated when compared with anesthetized dogs with intact kidneys. We conclude that the natriuretic response to an infusion of alpha-hANP is enhanced in dogs when anesthetized. Also, the natriuretic response was attenuated by renal denervation in dogs when anesthetized.

Interaction of the renal nerves and prostaglandins on the phosphaturic response to PTH in phosphate-deprived rats

1995 ◽  
Vol 268 (3) ◽  
pp. R731-R735 ◽  
Author(s):  
T. J. Berndt ◽  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Renal Denervation ◽  
Left Kidney ◽  
Fractional Excretion ◽  
Prostaglandin Synthesis ◽  
Acute Experiment ◽  
Renal Nerves ◽  
Prostaglandin I2 ◽  
Sham Surgery ◽  
Fractional Excretion Of Phosphate

Previous studies demonstrated that catecholamines modulate the phosphaturic response to parathyroid hormone (PTH) in normal rats. The present study was performed to determine the effect of unilateral renal denervation (DNX) and the interaction with prostaglandin synthesis on the blunted phosphaturic response to PTH in phosphate-deprived rats. One week before the acute experiment, rats were anesthetized, and the left kidney was denervated or sham surgery was performed. Rats were fed either a low-phosphate diet (LPD, 0.07%) or a normal-phosphate diet (NPD, 0.7%) for 2 days before the experiment. All rats were thyroparathyroidectomized (TPTX). Control clearances were taken from the left kidney 2 h after TPTX. PTH (33 U/kg + 1 U.kg-1.min-1) was infused for 45 min, and then the urine collections were repeated. In phosphate-deprived rats with an innervated kidney, PTH infusion resulted in a blunted phosphaturic response [changed fractional excretion of phosphate (delta FEPi) of 9.2 +/- 3.7%, n = 9] compared with rats fed NPD (delta FEPi 45.7 +/- 9.3%, n = 6) or those in the phosphate-deprived group with renal DNX (delta FEPi 23.6 +/- 5.0%, n = 12). Indomethacin pretreatment (3 mg/kg) markedly attenuated the phosphaturic response to PTH in phosphate-deprived rats with a denervated kidney (delta FEPi, 3.2 +/- 1.3%, n = 7) but not in animals fed an LPD with innervated kidneys or in rats fed an NPD. Infusion of Iloprost (2 ng.kg-1.min-1), a stable prostaglandin I2 analogue, in indomethacin-treated phosphate-deprived rats enhanced the phosphaturic response to PTH in rats with a denervated kidney (delta FEPi 17.3 +/- 3.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal nerves in the pathogenesis of hypertension in experimental animals and humans

1983 ◽  
Vol 245 (1) ◽  
pp. F1-F14 ◽  
Author(s):  
R. E. Katholi
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renovascular Hypertension ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Renal Tubules ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

Efferent renal innervation is composed of postganglionic sympathetic fibers to the renal arterioles, juxtaglomerular apparatus, and renal tubules. Increased efferent renal sympathetic nerve activity results in increased renal vascular resistance, renin release, and sodium retention. These responses from enhanced renal sympathetic activity contribute to normal cardiovascular homeostasis but could also facilitate the development of hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. Accordingly, interruption of the renal nerves should prevent the development of hypertension in animal models in which increased sympathetic nervous system activity has been implicated. Renal denervation delays the development of hypertension and results in greater sodium excretion in the Okamoto and New Zealand spontaneously hypertensive rat and in the DOCA-salt-treated rat, suggesting that these responses are due, at least in part, to loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in man. Recent studies indicate that the kidney is a sensory organ with mechano-receptive and chemoreceptive afferent renal nerves involved in renorenal and cardiovascular regulation. Renal denervation in established one-kidney one-clip and two-kidney one-clip Goldblatt hypertension in the rat and chronic coarctation in the dog results in an attenuation of the hypertension. The depressor effect of renal denervation in these models is not due to change in renin activity or sodium excretion but is associated with decreased activity of the sympathetic nervous system. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. The role of the afferent renal nerves in renovascular hypertension in humans warrants further study.

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