Denervated and intact kidney responses to exercise in the dog

1981 ◽  
Vol 51 (6) ◽  
pp. 1618-1624 ◽  
Author(s):  
J. Sadowski ◽  
R. Gellert ◽  
J. Kurkus ◽  
E. Portalaska
Keyword(s):  
Sodium Excretion ◽  
Filtration Rate ◽  
Renal Excretion ◽  
Urine Flow ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Intact Kidney ◽  
Exercise Induced ◽  
Induced Changes

In conscious female dogs exercise-induced changes in the function of the innervated and denervated kidney were studied by clearance techniques. The animals were prepared for experiments by chronic unilateral renal denervation and surgical division of the urinary bladder to enable separate urine collection from each kidney. A 20-min run on a treadmill at a speed of 2.6 m/s significantly decreased urine flow, osmolar clearance, sodium excretion, as well as clearances of exogenous creatinine and p-aminohippurate in the denervated kidney only. In dogs running at 3.6 m/s renal hemodynamics decreased significantly and similarly for both kidneys, whereas the fall in renal excretion was virtually limited to the denervated kidney. As glomerular filtration rate (GFR) was falling during exercise, sodium excretion per 100 ml GFR tended to increase in the innervated kidney, in contrast to an expected slight fall on the denervated side. This indicated a defect of tubular sodium reabsorption of the innervated kidney. On the whole, the data do not support an important mediatory role of renal nerves in the mechanism of renal function changes during exercise.

Activation of histamine H3 receptors inhibits renal noradrenergic neurotransmission in anesthetized dogs

2001 ◽  
Vol 280 (5) ◽  
pp. R1450-R1456 ◽  
Author(s):  
Tomoyuki Yamasaki ◽  
Isao Tamai ◽  
Yasuo Matsumura
Keyword(s):  
Receptor Antagonist ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Antidiuretic Action

To investigate the possible involvement of histamine H3 receptors in renal noradrenergic neurotransmission, effects of (R)alpha-methylhistamine (R-HA), a selective H3-receptor agonist, and thioperamide (Thiop), a selective H3-receptor antagonist, on renal nerve stimulation (RNS)-induced changes in renal function and norepinephrine (NE) overflow in anesthetized dogs were examined. RNS (0.5–2.0 Hz) produced significant decreases in urine flow and urinary sodium excretion and increases in NE overflow rate (NEOR), without affecting renal hemodynamics. When R-HA (1 μg · kg−1 · min−1) was infused intravenously, mean arterial pressure and heart rate were significantly decreased, and there was a tendency to reduce basal values of urine flow and urinary sodium excretion. During R-HA infusion, RNS-induced antidiuretic action and increases in NEOR were markedly attenuated. Thiop infusion (5 μg · kg−1 · min−1) did not affect basal hemodynamic and excretory parameters. Thiop infusion caused RNS-induced antidiuretic action and increases in NEOR similar to the basal condition. When R-HA was administered concomitantly with Thiop infusion, R-HA failed to attenuate the RNS-induced antidiuretic action and increases in NEOR. However, in the presence of pyrilamine (a selective H1-receptor antagonist) or cimetidine (a selective H2-receptor antagonist) infusion, R-HA attenuated the RNS-induced actions, similarly to the case without these antagonists. Thus functional histamine H3 receptors, possibly located on renal noradrenergic nerve endings, may play the role of inhibitory modulators of renal noradrenergic neurotransmission.

scholarly journals Role of ANG II in mediating somatosensory-induced renal nerve-dependent antinatriuresis in the rat

1998 ◽  
Vol 275 (1) ◽  
pp. R194-R202 ◽  
Author(s):  
Chunlong Huang ◽  
Edward J. Johns
Keyword(s):  
Sodium Excretion ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Renal Nerves ◽  
Ang Ii ◽  
Renal Nerve ◽  
Somatosensory Stimulation ◽  
Two Stages ◽  
The Brain

This study examined the renal nerve-dependent renal hemodynamic and tubular responses to somatosensory stimulation in the anesthetized rat by use of subcutaneously applied capsaicin when the action of ANG II was blocked peripherally or selectively within the brain. Activation of skin somatosensory receptors caused a transient reversible 10–15% increase in blood pressure, and while renal perfusion pressure was regulated at control levels, there was a transient fall in urine flow and sodium excretion even though both renal blood flow and glomerular filtration rate were unchanged. These reflexly induced excretory responses were abolished when the renal nerves were sectioned. Administration of the ANG II AT1-receptor antagonist, losartan, either intravenously at 3 or 10 mg/kg or locally into the lateral cerebroventricles at 15 μg plus 7.5 μg/h, had no effect on capsaicin-induced vasopressor responses but blocked the reductions in urine flow and sodium excretion. These findings are consistent with ANG II being involved in at least two stages in the reflex, one centrally and one at the periphery.

Role of prostaglandins and renal nerves in the renal actions of adrenomedullin

1997 ◽  
Vol 272 (2) ◽  
pp. F260-F266 ◽  
Author(s):  
M. Jougasaki ◽  
L. L. Aarhus ◽  
D. M. Heublein ◽  
S. M. Sandberg ◽  
J. C. Burnett
Keyword(s):  
Glomerular Filtration Rate ◽  
Renal Cell ◽  
Filtration Rate ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Intravenous Bolus ◽  
Hemodynamic Effects ◽  
Terminal Nephron

Adrenomedullin (ADM), originally discovered in human pheochromocytoma, is also of renal cell origin and has natriuretic and diuretic actions. The present study was designed to investigate the role of prostaglandins and renal nerves in the renal hemodynamic and natriuretic actions ofADM. ADM was administered intrarenally (1, 5 and 25 ng x kg(-1) x min(-1)) with and without prostaglandin inhibition (meclofenamate, 5 mg/kg intravenous bolus) in anesthetized normal mongrel dogs (n = 5, each). To elucidate the role of renal nerves, ADM was administered intrarenally to the denervated kidney in five dogs. ADM mediated a natriuretic action via increases in glomerular filtration rate and decreases in distal tubular sodium reabsorption, which was attenuated by renal denervation and completely abolished by prostaglandin inhibition. The renal vasodilatation induced by ADM was attenuated by meclofenamate, as well as by renal denervation, although not significantly. Additionally, renal nerves mediated hemodynamic effects of hypertension that were produced by intrarenal infusion of ADM. This study establishes an important mechanistic role for renal prostaglandins as a mediator of ADM-mediated natriuresis at the level of the glomerulus and terminal nephron.

Renal nerves and renal responses to volume expansion in conscious monkeys

1988 ◽  
Vol 255 (3) ◽  
pp. R388-R394 ◽  
Author(s):  
T. V. Peterson ◽  
B. A. Benjamin ◽  
N. L. Hurst
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Denervation ◽  
Renal Excretion ◽  
Isotonic Saline ◽  
Urine Flow ◽  
Renal Nerves ◽  
Blood Volume Expansion ◽  
Renal Responses

Experiments were performed in conscious macaque monkeys to determine the effect of renal denervation on the diuresis and natriuresis of blood volume expansion. When the kidneys were innervated, expansion of estimated blood volume by 20% with 3% dextran in isotonic saline caused increases in urine flow (V), from 0.28 +/- 0.07 ml/min to a peak response of 1.08 +/- 0.20 ml/min, absolute sodium excretion (UNaV), from 30.0 +/- 11.2 to 99.8 +/- 11.7 mueq/min, and fractional sodium excretion (FENa+), from 1.24 +/- 0.51 to 3.19 +/- 0.56%. The animals then underwent bilateral renal denervation and were volume expanded a second time 6-13 days postdenervation. Under this condition, V increased from 0.32 +/- 0.05 to 0.64 +/- 0.08 ml/min, UNaV, from 22.2 +/- 4.6 to 46.2 +/- 8.0 mueq/min, and FENa+, from 0.91 +/- 0.26 to 1.92 +/- 0.41%, these increases being significantly less than when the kidneys were innervated. These results demonstrate that the renal nerves play an important role in the nonhuman primate in mediating increases in renal excretion during hypervolemia.

The Role of Prostaglandins in Glucagon-Induced Natriuresis

1980 ◽  
Vol 58 (5) ◽  
pp. 393-401 ◽  
Author(s):  
M. A. Kirschenbaum ◽  
E. T. Zawada
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin E ◽  
Excretion Rates

1. Three groups of anaesthetized dogs were studied to determine the role of renal prostaglandins in glucagon-induced natriuresis. 2. Urine flow, sodium and prostaglandin E excretion rates increased significantly in the experimental kidney with glucagon infusion (0.20 μg/min) into the renal artery. These changes were completely reversed after the administration of either of two inhibitors of prostaglandin synthesis. 3. Infusion of glucagon (0.20 μg/min) after the administration of either of the prostaglandin synthetase inhibitors failed to increase either urine flow rate or sodium excretion above control values and failed to elevate urine prostaglandin E excretion rates. 4. Infusion of glucagon (0.75–1.25 μg/min) resulted in significant elevations in urine flow rate, glomerular filtration rate, renal plasma flow, urine sodium and prostaglandin E excretion rates. 5. The data presented indicate that the diuresis and natriuresis seen with the infusion of glucagon (0.20 μg/min) are accompanied by an increase in urine prostaglandin E excretion and are reversed by the administration of inhibitors of prostaglandin synthesis, suggesting that the increased urine flow and sodium excretion rates are dependent on prostaglandin-mediated mechanisms. The administration of glucagon in higher doses appears to be associated with alterations in electrolyte excretion and glomerular filtration rate, which presumably is related to factors other than prostaglandin synthesis and release.

Lack of a Role for the Renal Nerves in Renal Sodium Reabsorption in Conscious Dogs

1978 ◽  
Vol 54 (5) ◽  
pp. 567-572 ◽  
Author(s):  
M. D. Lifschitz
Keyword(s):  
Body Weight ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Fractional Sodium Excretion ◽  
Renal Sodium Reabsorption

1. Studies in anaesthetized animals suggest that the renal nerves have a role in the regulation of sodium excretion. Urinary sodium excretion decreases when the renal nerves are stimulated and increases after renal denervation or ganglionic blockade. In order to define the role of the renal nerves in the regulation of urinary sodium excretion in awake animals, dogs were prepared with one kidney denervated and the other intact and the bladder split so that urine could be collected from each kidney. Denervation was confirmed by kidney noradrenaline analysis (1·72 ± 0·29 vs 0·18 ± 0·12 nmol/g). 2. These dogs were studied awake with one of two protocols on each of two separate days. In protocol VH, volume expansion (5% body weight) was followed by haemorrhage of 2% body weight. Fractional sodium excretion fell from 4·7 ± 0·5 to 1·1 ± 0·2% on the denervated side and from 5·6 ± 0·6 to 1·4 ± 0·3% on the intact side. Inulin and p-aminohippurate clearance fell similarly on both sides. 3. In protocol HV, haemorrhage of 2% body weight was followed by blood replacement and volume expansion of 5% body weight. In this second protocol fractional sodium excretion during haemorrhage was 0·23 ± 0·07 and 0·24 ± 0·09% for denervated and intact kidneys respectively and increased to 2·04 ± 0·32 and 2·78 ± 0·60 after volume expansion. 4. In both protocols the denervated kidney was able to reabsorb sodium as well as the innervated kidney during haemorrhage and was able to increase fractional sodium excretion as well as the denervated kidney during volume expansion. These results suggest that the renal nerves do not have a significant role in the regulation of sodium excretion in conscious animals.

Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Osmotic Diuresis ◽  
Nacl Concentration ◽  
Proximal Tubular ◽  
Distal Tubules

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

Role of renal medullary adenosine in the control of blood flow and sodium excretion

1999 ◽  
Vol 276 (3) ◽  
pp. R790-R798 ◽  
Author(s):  
Ai-Ping Zou ◽  
Kasem Nithipatikom ◽  
Pin-Lan Li ◽  
Allen W. Cowley
Keyword(s):  
Blood Flow ◽  
Sodium Excretion ◽  
Renal Medulla ◽  
Urine Flow ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Medullary Blood Flow ◽  
Adenosine Concentration ◽  
Interstitial Infusion

This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 ± 5.2 nM, which was significantly higher than 55.6 ± 5.3 nM in the renal cortex ( n = 9). Renal medullary interstitial infusion of a selective A1antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol ⋅ kg−1 ⋅ min−1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX; 150 pmol ⋅ kg−1 ⋅ min−1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol ⋅ kg−1 ⋅ min−1( n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3receptor agonist, N 6-benzyl-5′-( N-ethylcarbonxamido)adenosine (300 pmol ⋅ kg−1 ⋅ min−1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects.

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.

Renal nerves and postprandial renal excretion in the conscious monkey

1991 ◽  
Vol 261 (5) ◽  
pp. R1197-R1203 ◽  
Author(s):  
T. V. Peterson ◽  
B. A. Benjamin ◽  
N. L. Hurst ◽  
C. G. Euler
Keyword(s):  
Urinary Excretion ◽  
Nonhuman Primate ◽  
Nasogastric Tube ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Renal Excretion ◽  
Renal Nerves ◽  
Electrolyte Excretion ◽  
Macaque Monkeys ◽  
High Sodium

Experiments were performed in conscious macaque monkeys to determine if the renal nerves are important in mediating postprandial increases in renal fluid-electrolyte excretion in this species. Monkeys were given a high-sodium meal via a nasogastric tube. Consecutive 10-min urine samples were taken during the 30-min time of meal administration and then 180 min postprandially. The experiment was performed both before and 10-14 days after each animal underwent renal denervation. Diuresis and natriuresis occurred under both renal-innervated and -denervated conditions. However, the amounts of urine and sodium excreted were less after renal denervation. For the total 210 min of measurements obtained after the meal was started, cumulative urine output was 95.0 +/- 26.4 ml and sodium excretion 7.18 +/- 1.74 meq in innervated kidneys vs. 56.7 +/- 7.0 ml (a 40% decrease; P less than 0.005) and 4.84 +/- 0.99 meq (a 33% decrease; P less than 0.01) after denervation. These results demonstrate that the renal nerves are important in the nonhuman primate for eliciting the postprandial changes in urinary excretion secondary to intake of a high-sodium meal.

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