Hemodynamic and renal responses to volume expansion in dogs with cardiac denervation

1988 ◽  
Vol 254 (6) ◽  
pp. F780-F786
Author(s):  
R. Pichet ◽  
J. Gutkowska ◽  
M. Cantin ◽  
M. Lavallee
Keyword(s):  
Plasma Levels ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Base Line ◽  
Aortic Constriction ◽  
Cardiac Denervation ◽  
Renal Responses

Hemodynamic responses, renal function, and plasma levels of immunoreactive atrial natriuretic factor (irANF) were examined following volume expansion (VE) in normal (N) conscious dogs and in conscious dogs with cardiac denervation (CD). Base-line urine flow was consistently greater (P less than 0.05) in dogs with CD (0.54 +/- 0.06 ml/min) than in N (0.29 +/- 0.03 ml/min) dogs but sodium excretion did not differ between N (2.80 +/- 0.58 mu eq.min-1.kg body wt-1) and CD (3.53 +/- 0.75 mu eq.min-1.kg-1) groups. With VE (18 ml/kg of 3% dextran in saline), mean arterial pressure (MAP) increased (P less than 0.01) by 16 +/- 3 from 103 +/- 4 mmHg in N dogs but did not change from pre-VE base line (103 +/- 2 mmHg) in dogs with CD. At 10 min after VE, urine flow increased more (P less than 0.01) in N dogs (1.39 +/- 0.24 ml/min) than in dogs with CD (0.26 +/- 0.09 ml/min). At that time, increases in sodium excretion were also greater (P less than 0.01) in N (9.13 +/- 1.96 mu eq.min-1.kg-1) dogs than in dogs with CD (1.06 +/- 0.68 mu eq.min-1.kg-1). With VE, increases in irANF plasma levels were not different in N dogs (40 +/- 12 from 34 +/- 5 pg/ml) and in dogs with CD (27 +/- 3 from 45 +/- 7 pg/ml). In dogs with CD, when MAP was increased by aortic constriction to mimic responses observed in N dogs, renal responses were similar to those of N dogs.(ABSTRACT TRUNCATEDAT 250 WORDS)

Natriuretic and diuretic effects of infusion of atrial natriuretic factor in conscious dogs

1989 ◽  
Vol 257 (4) ◽  
pp. F565-F573
Author(s):  
J. Ohanian ◽  
M. A. Young ◽  
Y. T. Shen ◽  
R. Gaivin ◽  
S. F. Vatner ◽  
...  
Keyword(s):  
Amino Acid ◽  
Arterial Pressure ◽  
Flow Rate ◽  
Plasma Levels ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Conscious Dogs ◽  
Natriuretic Factor

We studied the effects of 30-min infusions of the synthetic 25-amino acid atrial natriuretic factor [ANF-(102-126)] and the 28-amino acid ANF-(99-126) at 0.1 and 0.3 micrograms.kg-1.min-1 on urine flow rate, sodium excretion, and arterial pressure in conscious dogs. Each dose was administered on a separate day following a 1-h stabilization period. We also compared the effects of 60-min infusions of ANF, 0.01 micrograms.kg-1.min-1, or water infusion on separate days in conscious dogs. Arterial pressure was reduced in a dose-dependent fashion, reaching statistical significance at a dose of 0.3 micrograms.kg-1.min-1. During the 0.01-micrograms.kg-1.min-1 infusion, the plasma concentration of ANF rose approximately threefold (from 68 +/- 7 to 207 +/- 14 pg/ml), with no change in urine flow rate, sodium excretion, or arterial pressure. At a dose of 0.1 micrograms.kg-1.min-1, urine flow increased (P less than 0.05) by 0.41 +/- 0.15 ml/min, and sodium excretion rose by 72 +/- 24 mu eq/min, but not significantly, whereas plasma ANF levels rose to 1,236 +/- 229 pg/ml. At the highest dose of ANF (0.3 micrograms.kg-1.min-1) urine flow rose by 0.62 +/- 0.16 ml/min, P less than 0.05, and sodium excretion rose by 139 +/- 30 mu eq/min, P less than 0.05, whereas plasma levels of ANF rose to 2,436 +/- 320 pg/ml. In contrast, volume loading with dextran increased urine flow by 3.5 +/- 1.3 ml/min, P less than 0.05, and sodium excretion by 439 +/- 147 mu eq/min, P less than 0.05, whereas ANF rose to only 320 +/- 69 pg/ml. These results suggest that, in the conscious dog, ANF does not cause significant diuretic or natriuretic effects until plasma levels are markedly above those observed in physiological conditions. A possible explanation for the difference between this and previous studies is that the renal effects of ANF, at physiological plasma levels, are indirect and thus dependent on autonomic and hormonal (angiotensin, vasopressin, and aldosterone levels) factors governing the renal function of the animal.

Control of atrial natriuretic factor release in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. R947-R956 ◽  
Author(s):  
K. M. Verburg ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
D. Villarreal ◽  
R. C. Vari
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Base Line ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The aim of this study was to examine the changes in the concentration of plasma immunoreactive atrial natriuretic factor (iANF) that occur in response to expansion or depletion of the extracellular fluid volume in conscious dogs. The plasma iANF concentration was also measured postprandially after the ingestion of a meal containing 125 meq of sodium. Postprandial plasma iANF increased 45% (P less than 0.05) above the base-line concentration, and this increase was accompanied by a brisk natriuresis. After a low-sodium meal, however, plasma iANF and sodium excretion failed to increase. The plasma iANF concentration increased from 57 +/- 5 to 139 +/- 36 pg/ml (P less than 0.05) immediately after volume expansion with intravenous isotonic saline infusion (2.5% body wt) administered over a 30-min period; plasma iANF remained elevated at 90 +/- 14 pg/ml (P less than 0.05) for an additional 30 min before returning toward preinfusion levels. Plasma iANF decreased 45% from 78 +/- 17 to 43 +/- 7 pg/ml (P less than 0.05) in response to the administration of ethacrynic acid (2.0 mg/kg, iv bolus) that produced an estimated 15% depletion of intravascular volume. In additional experiments the infusion of synthetic alpha-human ANF at 100 and 300 ng X kg-1 X min-1 increased (P less than 0.05) both the plasma iANF concentration and the urinary excretion of iANF. This study demonstrates that the secretion of ANF is consistently influenced by changes in the extracellular fluid volume. Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal.

Reduced renal responses to an acute saline load in obese Zucker rats

1991 ◽  
Vol 261 (3) ◽  
pp. R712-R718 ◽  
Author(s):  
D. W. Zeigler ◽  
K. P. Patel
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Urine Flow ◽  
Reflex Response ◽  
Zucker Rats ◽  
Zucker Rat ◽  
Obese Zucker Rat ◽  
Obese Zucker Rats ◽  
Renal Responses

The purpose of this study was to determine if the reflex response to a saline load is altered in the obese Zucker rat. The obese Zucker rat is a genetic model of obesity and insulin-resistant diabetes that has been reported to have high blood pressure. We examined the reflux renal responses to volume expansion in both anesthetized obese and lean Zucker rats. Initial blood pressure was significantly elevated in the obese Zucker rats compared with the lean controls. Urine flow and sodium excretion from innervated and denervated kidneys were measured before and after volume expansion with normal saline. Volume expansion resulted in significantly less urine flow and sodium excretion in the obese than the lean Zucker rats. This response was evident in both the intact and denervated kidneys. Rats were then infused with atrial natriuretic peptide (ANP) to determine if natriuretic and diuretic responses were altered in these rats. The diuretic action of ANP was not significantly reduced in the obese Zucker rat. However, the natriuretic action of ANP was significantly attenuated in the obese rats. These results indicate that the reflux response to an acute saline load is attenuated in the obese Zucker rat and that this decreased response may be due to a reduction in the direct action of ANP on the kidney.

Attenuated renal responses to atrial natriuretic factor in streptozotocin-induced diabetic rats

1990 ◽  
Vol 68 (3) ◽  
pp. 425-430 ◽  
Author(s):  
Kaushik P. Patel ◽  
Ping L. Zhang
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Urine Flow ◽  
Control Group ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Glucose Levels ◽  
Natriuretic Factor ◽  
Renal Responses ◽  
Atrial Natriuretic

To determine whether the renal responses to atrial natriuretic factor (ANF) are altered in the diabetic state, the diuretic and natriuretic responses to ANF (0.25 μg∙kg−1∙min−1, i.v.) were measured in streptozotocin (STZ) induced diabetic (DIA) rats. Urine flow and sodium excretion were measured before and after ANF from innervated and denervated kidneys in anesthetized (Inactin 0.1 g/kg, i.p.) control and DIA rats (Sprague–Dawley rats injected with vehicle or STZ 65 mg/kg, i.p., respectively, 2 weeks prior to the experiment). Blood glucose levels were significantly elevated in the DIA group compared with the control group. ANF produced a significantly blunted diuresis and natriuresis in DIA rats compared with control rats. In addition, reducing the hyperglycemia in DIA rats by treatment with insulin (third group) reversed the blunted urine flow and sodium excretion responses to ANF. This study demonstrates that (i) there is a blunted natriuresis and diuresis to ANF in the STZ-induced DIA rats, and (ii) restoring the glucose levels to normal by insulin treatment in the DIA rats normalized the renal responses to ANF.Key words: diuresis, natriuresis, renal nerves, atrial natriuretic factor.

Atrial peptide potentiates renal responses to volume expansion in conscious dogs

1989 ◽  
Vol 256 (1) ◽  
pp. R284-R289
Author(s):  
C. H. Metzler ◽  
D. J. Ramsay
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Physiological Dose ◽  
Peptide Secretion ◽  
Renal Responses ◽  
Dose Dependent

Experiments were performed to compare the renal responses to atrial peptide infusion in conscious dogs with normal and expanded extracellular fluid volumes to test the hypothesis that the renal responses to atrial peptide infusions are dependent on the prevailing fluid and electrolyte status in the animal. Atrial peptide-(99-126) was infused intravenously in doses of either 0, 5, 25, or 100 ng.kg-1.min-1 in conscious dogs prepared with chronic catheters in the femoral artery and vein and the urinary bladder. In dogs with normal extracellular fluid volume, atrial peptide caused small increases in urinary sodium excretion with the high physiological (25 ng.kg-1.min-1) and pharmacological (100 ng.kg-1.min-1) doses. Urine volume and potassium excretion were increased only at the highest pharmacological dose. In contrast, atrial peptide infusion in dogs that were volume expanded by infusion of hypertonic saline showed dramatic, dose-dependent increases in sodium excretion and urine flow with all doses tested. The low, physiological dose of atrial peptide (5 ng.kg-1.min-1) increased sodium excretion and urine flow rate in volume-expanded dogs more than the pharmacological dose in normal dogs (n = 4). These results demonstrate that the renal responses to atrial peptide infusion are potentiated in dogs that are volume expanded and suggest that under conditions where atrial peptide secretion would be enhanced, small changes in plasma atrial peptide concentration can have significant effects on renal function.

Nitric oxide and renal effects of volume expansion in conscious monkeys

1997 ◽  
Vol 272 (4) ◽  
pp. R1033-R1038 ◽  
Author(s):  
T. V. Peterson ◽  
A. B. Carter ◽  
R. A. Miller
Keyword(s):  
Nitric Oxide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Control Volume ◽  
No Synthase ◽  
Urine Flow ◽  
Primate Species ◽  
Constant Infusion ◽  
Synthase Inhibitor ◽  
Renal Responses

Experiments were performed to determine the effects of nitric oxide (NO) synthase inhibition on the renal responses to volume expansion in conscious cynomolgus monkeys. All animals were volume expanded with 3% dextran in normal saline under three conditions: 1) during a control state, 2) during constant infusion of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 30 microg x kg(-1) x min(-1)), and 3) during simultaneous infusion of L-NAME and excess NO substrate L-arginine (0.6 mg x kg(-1) x min(-1)). The control volume expansion increased urine flow from 0.27 +/- 0.05 to 0.94 +/- 0.28 ml/min and sodium excretion from 21 +/- 9 to 95 +/- 26 microeq/min. During L-NAME infusion, these responses were attenuated in that urine flow only increased from 0.13 +/- 0.03 to 0.28 +/- 0.09 ml/min and sodium excretion from 13 +/- 8 to 35 +/- 23 microeq/min. Addition of L-arginine to the L-NAME infusion abolished these renal excretory effects of L-NAME alone. With combined L-NAME/L-arginine, volume expansion increased urine flow from 0.37 +/- 0.23 to 1.09 +/- 0.23 ml/min and sodium excretion from 38 +/- 27 to 150 +/- 24 microeq/min, responses similar to control. L-Arginine also markedly attenuated the effect of L-NAME to increase mean arterial pressure and abolished the L-NAME decreases in creatinine and p-aminohippurate clearances. However, an L-NAME-induced bradycardia could only be partially reversed. These results demonstrate that a functioning NO system may be important in mediating normal renal responses to volume expansion in this primate species.

Pentobarbital potentiates natriuretic response to acute volume expansion in monkeys

1988 ◽  
Vol 254 (5) ◽  
pp. R727-R729
Author(s):  
J. P. Gilmore ◽  
K. G. Cornish ◽  
M. W. Barazanji
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Urine Flow ◽  
Inhibitory Influence ◽  
Lower Blood Pressure ◽  
Lower Blood ◽  
Renal Tubular ◽  
Renal Responses ◽  
Conscious Animals ◽  
Dextran Solution

We determined the influence of pentobarbital sodium on the renal responses of the monkey to acute intravascular volume expansion. Before volume expansion, the anesthetized animals had a significantly lower blood pressure and creatinine clearance and a significantly higher urine flow and sodium excretion than the conscious animals. After volume expansion with an isotonic, isoncotic, dextran solution, sodium excretion and urine flow increased significantly in both groups of animals. However, both responses were significantly greater in the anesthetized animals. The greater natriuresis in the anesthetized animals was associated with a greater fractional sodium excretion than in the conscious animals. The potentiated response of the anesthetized animal may be the result of a direct renal tubular effect of pentobarbital and/or the result of the anesthetic removing an inhibitory influence on sodium excretion.

Renal response to volume expansion in atrial-appendectomized dogs

1987 ◽  
Vol 253 (5) ◽  
pp. R786-R793
Author(s):  
B. A. Benjamin ◽  
C. H. Metzler ◽  
T. V. Peterson
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Control Period ◽  
Urine Flow ◽  
Central Venous ◽  
Renal Response ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs

The purpose of this study was to determine whether chronic removal of the atrial appendages alters the renal response to volume expansion (VE) in anesthetized dogs. Chronic bilateral atrial appendectomy (ATX) was performed in 10 animals. Six animals served as sham-operated controls (S). The animals were studied 10-14 days after chronic surgery. The protocol consisted of a 20-min control period followed by isochemic VE (20%) and 120 min of post-VE measurements. The dogs were studied a second time, 2 wk later, after acute bilateral cervical vagotomy. Results from the vagi-intact study showed that VE caused a diuresis, natriuresis, and increase in fractional sodium excretion in ATX that did not differ from the response observed in S. VE also caused equivalent increases in central venous and mean arterial pressures in S and ATX. Atrial appendectomy, however, failed to significantly attenuate the increase in atrial natriuretic factor (ANF) after VE. Plasma ANF increased from 27.2 +/- 4.8 to 47.0 +/- 7.3 pg/ml in ATX and from 27.2 +/- 7.8 to 59.0 +/- 17.9 pg/ml in S. After vagotomy, VE caused transient increases in urine flow and sodium excretion. The changes in central venous and mean arterial pressures were not different from the vagi-intact study and vagotomy did not affect the increase in ANF after VE. Circulating ANF levels increased from 26.4 +/- 5.5 to 75.0 +/- 14.0 pg/ml in ATX and from 28.1 +/- 5.7 to 73.0 +/- 22.6 pg/ml in S. These results demonstrate that, in the dog, bilateral ATX does not alter the renal response to volume expansion or attenuate the increase in ANF. In addition, these results show that vagal pathways are not required for the release of ANF and that vagotomy fails to uncover any effect of atrial appendectomy on renal function.

Abnormal renal hemodynamics and pressure-natriuresis relationship in Dahl salt-sensitive rats

1986 ◽  
Vol 251 (1) ◽  
pp. F57-F65 ◽  
Author(s):  
R. J. Roman
Keyword(s):  
Arterial Pressure ◽  
Plasma Levels ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Pressure Natriuresis ◽  
Renal Responses

The renal responses to changes in renal perfusion pressure (RPP) were compared in Dahl salt-resistant (R) rats and in prehypertensive and hypertensive Dahl salt-sensitive (S) rats to determine whether an abnormality in the pressure diuresis response is involved in the development of this form of hypertension. Possible differences in the neural and endocrine background to the kidney of S and R rats were eliminated by denervating the kidney and by holding plasma levels of vasopressin, aldosterone, corticosterone, and norepinephrine fixed by intravenous infusion. Arterial pressure averaged 124 +/- 1 mmHg in R rats, 133 +/- 1 mmHg in prehypertensive S rats, and 158 +/- 2 mmHg in hypertensive S rats. Control renal blood flows (RBF) and glomerular filtration rates (GFR) were not significantly different in the three groups. RBF was autoregulated over a range of pressures from 80 to 160 mmHg in normotensive S and R rats. GFR was autoregulated at pressures greater than 100 mmHg in R rats and greater than 120 mmHg in prehypertensive S rats. In contrast, RBF was only autoregulated at pressures greater than 110 mmHg in hypertensive Dahl S rats, and GFR was significantly reduced from control when RPP was lowered below 150 mmHg. In R rats, increasing RPP from 100 to 150 mmHg produced a fivefold increase in urine flow and sodium excretion. In prehypertensive or hypertensive Dahl S rats the slopes of the relationships between urine flow, sodium excretion, and RPP were less than half of those seen in R rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Sign in / Sign up

Export Citation Format

Share Document