Dopaminergic regulation of natriuretic response to acute volume expansion in dogs

1985 ◽  
Vol 68 (3) ◽  
pp. 263-269 ◽  
Author(s):  
M. McClanahan ◽  
J. R. Sowers ◽  
F. W. J. Beck ◽  
P. K. Mohanty ◽  
T. McKenzie
Keyword(s):  
Volume Expansion ◽  
Chloride Solution ◽  
Renal Excretion ◽  
Urinary Sodium Excretion ◽  
Saline Infusion ◽  
Decarboxylase Inhibitor ◽  
Hormonal Responses ◽  
Vascular Volume ◽  
Solution Saline ◽  
Dopaminergic Regulation

1. Effects of carbidopa, a dopa (3,4-dihydroxy-phenylamine) decarboxylase inhibitor, on the renal, haemodynamic and hormonal responses to acute volume expansion were examined in six healthy mongrel dogs which were infused intravenously with 0.9% sodium chloride solution (saline; 30 ml h−1 kg−1) over 2 h. 2. Saline infusion studies were performed in the absence (control) and in the presence of carbidopa given by nasogastric tube in a dose of 1 mg/kg every 8 h beginning 24 h before the infusion. 3. Saline infusion resulted in an increase in renal excretion of dopamine (3,4-dihydroxy-phenylethylamine) and a decrease in renal excretion of noradrenaline. 4. Carbidopa treatment decreased urinary sodium excretion and eliminated the increase in renal production of dopamine in response to saline infusion without affecting renal or haemodynamic response to acute vascular volume expansion with saline. 5. Carbidopa treatment obliterated the suppression of aldosterone produced by saline infusion. 6. Thus, dopamine appears to play a significant role in mediating both the natriuretic and aldosterone response to acute volume expansion.

The Release of Renal Prostaglandins during Saline Infusion in Normal and Hypertensive Subjects

1975 ◽  
Vol 49 (5) ◽  
pp. 459-463 ◽  
Author(s):  
N. Papanicolaou ◽  
M. Safar ◽  
A. Hornych ◽  
F. Fontaliran ◽  
Y. Weiss ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Flow ◽  
Chloride Solution ◽  
Renal Plasma Flow ◽  
Saline Infusion ◽  
Urinary Output ◽  
Prostaglandin Release ◽  
Before And After ◽  
Solution Saline ◽  
Pressure Changes

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.

Comparison of the Effects on Urinary Sodium Excretion of Indomethacin and of Carbidopa in normal Volunteers given an Intravenous Saline Infusion

1997 ◽  
Vol 92 (4) ◽  
pp. 409-414
Author(s):  
G. S. Stokes ◽  
J. C. Monaghan ◽  
D. N. Pillai
Keyword(s):  
Volume Expansion ◽  
Randomized Study ◽  
Plasma Concentrations ◽  
Urinary Sodium Excretion ◽  
Saline Infusion ◽  
Normal Volunteers ◽  
Intravenous Saline ◽  
Urinary Dopamine ◽  
Natriuretic Effect ◽  
Renal Tubular

1. Dopamine and prostaglandins are putative endogenous natriuretic hormones. The role of each in facilitating natriuresis induced by intravenous saline infusion was examined in normal volunteers in relation to administration of carbidopa, a dopadecarboxylase inhibitor, and indomethacin, an inhibitor of prostaglandin synthetase. 2. In a placebo-controlled, randomized study, 13 subjects received carbidopa (100 mg) and 12 received indomethacin (50 mg). Proximal and distal renal tubular Na+ reabsorption were determined using exogenous lithium clearance. 3. On the control day, 2 litres of 0.9% saline (308 mmol Na+) given intravenously in 3 h, resulted in volume expansion and natriuresis. Carbidopa reduced the urinary dopamine/noradrenaline ratio but showed no anti-natriuretic effect and no effect on fractional Na+ reabsorption. Indomethacin diminished natriuresis and increased distal fractional Na+ reabsorption in proportion to the anti-natriuretic effect. 4. The changes in plasma concentrations of albumin, aldosterone, atrial natriuretic peptide and renin activity associated with volume expansion were not modified by either carbidopa or indomethacin. Urinary prostaglandin E2 excretion was decreased transiently by indomethacin and was unaffected by carbidopa. 5. This study suggests that prostaglandins may modulate urinary Na+ excretion during saline-induced natriuresis through inhibition of distal tubular Na+ reabsorption. No role for free dopamine as a modulator of renal Na+ handling could be assigned on the basis of the findings with carbidopa.

Atrial natriuretic peptide – cyclic GMP coupling and urinary sodium excretion during acute volume expansion in man

1990 ◽  
Vol 68 (4) ◽  
pp. 535-538 ◽  
Author(s):  
Giuseppe A. Sagnella ◽  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Graham A. MacGregor ◽  
David G. Shirley ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cyclic Gmp ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Saline Infusion ◽  
Atrial Natriuretic

The present study examines hormonal and renal responses to acute volume expansion in normal man, with particular emphasis on the atrial natriuretic peptide (ANP) – cyclic GMP coupling. Two liters of isotonic saline were infused into eight normotensive male subjects over a 1-h period. Plasma and urinary measurements were made before, during, and up to 300 min after the start of the saline infusion. With the initial increase in urinary sodium excretion there were increases in plasma ANP and plasma cyclic GMP, which reached maximum levels at 15 min after the end of the saline infusion. Urinary cyclic GMP increased gradually during saline infusion up to approximately 60 min after the end of the infusion. Plasma ANP and plasma and urinary cyclic GMP excretion gradually declined thereafter. By contrast, urinary sodium excretion remained elevated up to the end of the observation period. The saline infusion was associated with marked reductions in plasma renin activity and aldosterone, which persisted up to the end of the study. These results suggest a coupling between the increases in plasma ANP, the production of cyclic GMP, and urinary sodium excretion, in particular during the initial renal response to acute volume expansion. However, other mechanisms including the suppression of the rennin–angiotensin–aldosterone system may become increasingly important in the later natriuretic response to acute volume expansion.Key words: atrial natriuretic peptide, cyclic GMP, sodium, renal, human.

Direct renal interstitial volume expansion causes exaggerated natriuresis in SHR

1991 ◽  
Vol 261 (4) ◽  
pp. F567-F570 ◽  
Author(s):  
A. A. Khraibi
Keyword(s):  
Volume Expansion ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Interstitium ◽  
Time Control ◽  
Arterial Blood ◽  
Interstitial Volume ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto ◽  
Second Period

In Okamoto spontaneously hypertensive rats (SHR), elevated arterial blood pressure is not transmitted to the renal interstitium, and therefore pressure natriuretic and diuretic responses are attenuated. The objective of this study was to determine the effect of increasing renal interstitial hydrostatic pressure (RIHP) by direct renal interstitial volume expansion (DRIVE) on natriuresis and diuresis of SHR and Wistar-Kyoto rats (WKY). Unilateral nephrectomy and implantation of two polyethylene (PE) matrices were performed 3-4 wk before the acute experiment. Four groups of rats, two experimental and two time control, were used. A control clearance period was taken in all groups. In experimental groups and at the beginning and middle of the second period DRIVE was accomplished by bolus injection of a solution of 2.5% human albumin in saline directly into interstitium through one of the PE matrices. In time-control groups saline was infused in renal interstitium at the beginning of the second period. The second PE matrix was used to continuously measure RIHP in all groups. In experimental groups, DRIVE produced a significant increase in RIHP from 3.8 +/- 0.4 to 5.7 +/- 0.8 mmHg (P less than 0.05) in SHR and 4.3 +/- 0.4 to 7.1 +/- 0.5 mmHg (P less than 0.05) in WKY. In both groups the significant increase in RIHP was associated with significant increases in urinary sodium excretion (UNaV), fractional excretion of sodium (FENa), and urine flow rate (V).(ABSTRACT TRUNCATED AT 250 WORDS)

Preoptic-hypothalamic periventricular lesions reduce natriuresis to volume expansion

1983 ◽  
Vol 244 (1) ◽  
pp. R51-R57 ◽  
Author(s):  
S. L. Bealer ◽  
J. R. Haywood ◽  
K. A. Gruber ◽  
V. M. Buckalew ◽  
G. D. Fink ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Third Ventricle ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Toad Bladder ◽  
Arterial Blood ◽  
Electrolytic Ablation ◽  
High Level ◽  
Periventricular Lesions

The present experiment was designed to determine if electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) altered the natriuresis typically seen during isotonic volume expansion. Control and AV3V-lesioned rats received intravenous infusions of 0.9% NaCl at 0.5 ml/min until 10% body weight was given. Arterial blood pressure was monitored, and urine was collected throughout the experiment. Following expansion, blood was processed for analysis of natriuretic hormonelike activity by chromatographic separation of plasma extracts followed by measuring antinatriferic activity across the isolated toad bladder. Urinary sodium excretion and urine volume during expansion were significantly less in rats with lesions surrounding the AV3V region than in control rats. Toad bladder bioassay showed a high level of natriuretic hormonelike activity in control animals following volume expansion, but no natriuretic hormonelike activity in plasma from volume-expanded rats with AV3V lesions. These data demonstrate that AV3V periventricular ablation attenuates the natriuresis induced by isotonic-volume expansion. In addition, preliminary results indicate the AV3V region may be a central site critical for natriuretic hormonelike activity and control of extracellular fluid volume.

Role of atrial natriuretic peptide in volume-expansion natriuresis

1986 ◽  
Vol 251 (2) ◽  
pp. R310-R313 ◽  
Author(s):  
T. R. Schwab ◽  
B. S. Edwards ◽  
D. M. Heublein ◽  
J. C. Burnett
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Right Atrial ◽  
Fractional Excretion Of Sodium

Studies were performed to investigate the role of circulating atrial natriuretic peptide (ANP) in acute volume-expansion natriuresis. Sham-operated (SHAM, n = 6) and right atrial appendectomized (ATRX, n = 12) anesthetized rats underwent acute volume expansion with isoncotic albumin. After equilibration and control periods, volume expansion increased urine flow rate, urinary sodium excretion, fractional excretion of sodium, and circulating ANP. Absolute increases in urine flow rate (delta 46 +/- 4 SHAM; delta 25 +/- 5 microliter/min ATRX), urinary sodium excretion (delta 9.48 +/- 1.01 SHAM; delta 4.77 +/- 1.03 mueq/min ATRX), fractional excretion of sodium (delta 3.16 +/- 0.53 SHAM; delta 1.65 +/- 0.32% ATRX), and ANP (delta 303.3 +/- 35.9 SHAM; delta 156.6 +/- 26.0 pg/ml ATRX) were significantly reduced by right atrial appendectomy. No significant differences in mean arterial pressure, central venous pressure, or glomerular filtration rate during volume expansion were observed between groups. These studies support the hypothesis that right atrial appendectomy in the rat attenuates acute volume expansion-induced increases in circulating ANP and urinary sodium excretion and that the natriuresis of acute volume expansion is mediated in part by an increase in circulating ANP.

Prostaglandin blockade blunts the natriuresis of elevated renal interstitial hydrostatic pressure

1988 ◽  
Vol 254 (4) ◽  
pp. F507-F511 ◽  
Author(s):  
D. Pawlowska ◽  
J. A. Haas ◽  
J. P. Granger ◽  
J. C. Romero ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Left Kidney ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Fractional Sodium Excretion ◽  
Interstitial Volume ◽  
Inhibition Of Prostaglandin Synthesis

Previous studies have shown that renal interstitial volume expansion (RIVE) increases renal interstitial hydrostatic pressure and urinary sodium excretion. In the present study we investigated whether blockade of prostaglandin synthesis inhibits the increase in fractional sodium excretion induced by RIVE. Expansion of the renal interstitial volume was achieved by injecting 50 microliters of 2.5% albumin solution into a polyethylene matrix chronically implanted in the left kidney. Fractional sodium excretion (FENa), renal interstitial hydrostatic pressure (PI), and urinary prostaglandin excretion (UPGE2) were measured before and after RIVE in eight control, seven meclofenamate-treated, and eight indomethacin-treated rats. RIVE in the control animals resulted in significant increases in PI (delta + 4.2 +/- 0.8 mmHg), in FENa (delta + 1.02 +/- 0.27%), and in UPGE2 (% delta + 150 +/- 38%) without significant changes in glomerular filtration rate. Inhibition of prostaglandin synthesis with meclofenamate or indomethacin attenuated the natriuretic response and blocked the increase in UPGE2 associated with RIVE. In summary, direct increases in renal interstitial hydrostatic pressure increase UPGE2 and urinary sodium excretion. This natriuretic response is markedly diminished by inhibition of prostaglandin synthesis. These studies suggest that prostaglandin synthesis may have an important role in mediating the natriuretic effect of increased renal interstitial hydrostatic pressure during renal interstitial volume expansion.

SEPSIS DOES NOT ALTER PLASMA VOLUME EXPANSION (PVE) IN RESPONSE TO 0.9% SALINE INFUSION IN SHEEP

1999 ◽  
Vol 27 (Supplement) ◽  
pp. 49A
Author(s):  
K.I. Brauer ◽  
D.S. Prough ◽  
J.B. Clifton ◽  
L.D. Traber ◽  
D.L. Traber
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Saline Infusion ◽  
Plasma Volume Expansion
Sign in / Sign up

Export Citation Format

Share Document