Hormonal interactions and renal function during mechanical ventilation and ANF infusion in humans

1991 ◽  
Vol 70 (1) ◽  
pp. 287-292 ◽  
Author(s):  
P. Andrivet ◽  
S. Adnot ◽  
S. Sanker ◽  
P. E. Chabrier ◽  
I. Macquin-Mavier ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Renal Function ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Positive End Expiratory Pressure ◽  
Hormonal Responses ◽  
Fractional Excretion Of Sodium

To investigate the influence of atrial natriuretic factor (ANF) on renal function during mechanical ventilation (MV), we examined the renal and hormonal responses to synthetic human ANF infusion in eight patients during MV with zero (ZEEP) or 10 cmH2O positive end-expiratory pressure (PEEP). Compared with ZEEP, MV with PEEP was associated with a reduction in diuresis (V) from 208 +/- 51 to 68 +/- 11 ml/h (P less than 0.02), in natriuresis (UNa) from 12.4 +/- 3.3 to 6.2 +/- 2.1 mmol/h (P less than 0.02), and in fractional excretion of sodium (FENa) from 1.07 +/- 0.02), 0.21 to 0.67 +/- 0.17% (P less than 0.02) and with an increase in plasma renin activity (PRA) from 4.83 +/- 1.53 to 7.85 +/- 3.02 ng.ml-1.h-1 (P less than 0.05). Plasma ANF levels markedly decreased during PEEP in four patients but showed only minor changes in the other four patients, and mean plasma ANF levels did not change (163 +/- 33 pg/ml during ZEEP and 126 +/- 30 pg/ml during PEEP). Glomerular filtration rate and renal plasma flow were unchanged. Infusion of ANF (5 ng.kg-1.min-1) during PEEP markedly increased V and UNa by 110 +/- 61 and 107 +/- 26%, respectively, whereas PRA decreased from 7.85 +/- 3.02 to 4.40 +/- 1.5 ng.ml-1.min-1 (P less than 0.05). In response to a 10 ng.kg-1.min-1 ANF infusion, V increased to 338 +/- 79 ml/h during ZEEP but only to 134 +/- 45 ml/h during PEEP (P less than 0.02), whereas UNa increased, respectively, to 23.8 +/- 5.3 and 11.3 +/- 3.3 mmol/h (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Haemodynamic and Renal Effects of Dopexamine after Cardiac Surgery in Children

1996 ◽  
Vol 24 (4) ◽  
pp. 435-439 ◽  
Author(s):  
W. Habre ◽  
M. Beghetti ◽  
C. Roduit ◽  
E. Girardin ◽  
M. Vallotton ◽  
...  
Keyword(s):  
Heart Rate ◽  
Renal Function ◽  
Cardiac Surgery ◽  
Renal Plasma Flow ◽  
Stroke Volume Index ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Volume Index ◽  
Renal Effects ◽  
Fractional Excretion Of Sodium

Dopexamine hydrochloride, a synthetic dopamine analog with predominantly beta and delta agonist properties, has been shown to improve cardiac performance and renal function in adults with heart failure. This study was designed to investigate the haemodynamic and renal effects of dopexamine in children after cardiac surgery. Seven children were selected in whom a need for postoperative vasodilation after cardiac surgery was anticipated. Haemodynamics and renal function were determined under baseline conditions and during a continuous infusion of dopexamine at 2 and 6 μg.kg-1.min-1 for 90 minutes, the sequence being randomized for the initial dose. Cardiac output was measured by thermodilution and glomerular filtration rate (GFR) and renal plasma flow (RPF) by the clearances of inulin and para-aminohippurate respectively. Dopexamine induced a dose-related increase in cardiac index (CI) expressed as mean (SD) from 3.5 (0.7) to 3.9 (0.76) and 4.5 (0.8) l.min.-1m-2 (both P<0.05), and in heart rate (HR) from 107 (17) to 122 (17) and 136 (17) beats.min-1 (P<0.05). Stroke volume index (SVI) and mean systemic pressure were unchanged, but pulmonary wedge pressure decreased from 14 (3) to 11 (4) and 12 (3) mmHg (both P<0.05). Systemic vascular resistances (SVR) decreased from 24 (7) to 20 (5) mmHg.l-1.min-1.m-2 (P<0.05), with dopexamine 6 μg.kg-1.min-1. Renal blood flow (RBF) increased from 319 (113) to 441 (230) and 410 (138) ml.min-1.m-2 (both P<0.05), GFR from 115 (32) to 142 (34) and 146 (29) ml.min-1.1.73m-2 (both P<0.05), urine output and fractional excretion of sodium respectively from 3.12 (2) to 7.16 (8) and 7.21 (6) ml.kg-1 (both P<0.05) and from 2.24 (1) to 4.25 (3.4) (P<0.05) and 3.15 (3.1)% (n.s.). The fraction of CI delivered to the kidneys, the fraction of RBF filtered in the kidneys, plasma renin activity and aldosterone levels remained unchanged. In children after cardiac surgery, dopexamine increases CI at the expense of a concomitant increase in heart rate and demonstrates few selective vascular systemic or intrinsic renal actions.

Role of renal nerves in response to volume expansion in conscious newborn lambs

1989 ◽  
Vol 257 (6) ◽  
pp. R1519-R1525 ◽  
Author(s):  
F. G. Smith ◽  
T. Sato ◽  
O. J. McWeeny ◽  
L. Torres ◽  
J. E. Robillard
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Glomerular Filtration ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renal Nerves

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.

Urodilatin, a natriuretic factor from kidneys, can modify renal and cardiovascular function in men

1990 ◽  
Vol 259 (5) ◽  
pp. F832-F838 ◽  
Author(s):  
H. Saxenhofer ◽  
A. Raselli ◽  
P. Weidmann ◽  
W. G. Forssmann ◽  
A. Bub ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Factor ◽  
Healthy Subjects ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Cardiovascular Function ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Amino Acid Residues ◽  
Natriuretic Factor

Urodilatin is a newly identified analogue of human atrial natriuretic factor-(99-126) [ANF-(99-126)], which has recently been isolated from human urine and has 32 amino acid residues [ANF-(95-126)]. To investigate renal and cardiovascular effects in men, eight healthy subjects received injections of 25, 50, and 100 micrograms urodilatin iv compared with 50 micrograms ANF-(99-126) and placebo. Blood pressure decreased (P less than 0.05) after 50 micrograms ANF-(99-126), whereas urodilatin lowered diastolic blood pressure only at the highest dose (P less than 0.01). Heart rate increased (P less than 0.05-0.01) dose dependently after urodilatin injections. Glomerular filtration rate rose after 100 micrograms (from 120 +/- 3 to 156 +/- 7 ml.min-1.1.73 m-2, P less than 0.001) and 50 micrograms urodilatin (from 116 +/- 7 to 149 +/- 13 ml.min-1.1.73 m-2, P less than 0.01) but not after 25 micrograms urodilatin, ANF-(99-126), or placebo. Effective renal plasma flow was not significantly modified. Diuresis and excretion of sodium, chloride, and guanosine 3',5'-cyclic monophosphate increased (P less than 0.001) dose dependently; effects of 25 micrograms urodilatin equaled those of 50 micrograms ANF-(99-126). Plasma renin, aldosterone, and catecholamines were unchanged. We conclude that urodilatin can acutely modify renal and cardiovascular function in men and seems to exert more potent renal effects than ANF-(99-126).

Unimpaired excretion of an acute salt load in conscious hypoproteinaemic dogs

1988 ◽  
Vol 75 (3) ◽  
pp. 271-276 ◽  
Author(s):  
J. A. Joles ◽  
H. A. Koomans ◽  
P. Boer ◽  
E. J. Dorhout Mees
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Protein ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Sodium Reabsorption ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium

1. The role of hypoproteinaemia in the sodium retention seen in conditions such as the nephrotic syndrome is incompletely known. 2. To define the influence of severe hypoproteinaemia on kidney function, we studied the effect of an intravenous infusion of an isotonic saline load (133 mmol of sodium), as 1 litre of Ringer lactate solution, on sodium excretion and renal haemodynamics in conscious dogs before and after reduction of plasma protein from 68 ± 3 to 36 ±2 g/l by repeated plasmapheresis and a low protein diet. 3. During hypoproteinaemia, 2 days after a period of plasmapheresis, glomerular filtration rate and effective renal plasma flow were lower than in the control study. After the sodium load, both rose to values nearly identical with the pre-infusion levels found in normoproteinaemia, the filtration fraction remaining unchanged. This contrasted with the rise in filtration fraction after expansion in normoproteinaemia, where filtration fraction increased from 32 to 39% due to a rise in glomerular filtration rate. 4. After expansion, natriuresis rose to similar levels in normoproteinaemia (0.18 ±0.06 mmol/min) and hypoproteinaemia (0.20 ± 0.06 mmol/min), and increments in fractional excretion of sodium, potassium and chloride were also similar. However, baseline excretion was higher in the hypoproteinaemic dogs due to their overhydrated condition in this period immediately after plasmapheresis. 5. The fractional excretion of lithium, an alleged marker of proximal tubular sodium reabsorption, rose to comparable levels. 6. Hence, both the increase in filtration and decrease in reabsorption of sodium after an isotonic saline load are not affected by severe reduction in plasma protein concentration. Apparently, the pathways to augment natriuresis after acute expansion function normally in hypoproteinaemia.

Effect of inhibition of MAO and COMT on intrarenal dopamine and serotonin and on renal function

2001 ◽  
Vol 280 (1) ◽  
pp. R248-R254 ◽  
Author(s):  
Yongqing Wang ◽  
Theresa J. Berndt ◽  
Jennifer M. Gross ◽  
Michael A. Peterson ◽  
Mathew J. So ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Monoamine Oxidase ◽  
Filtration Rate ◽  
Interstitial Fluid ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Arterial Blood ◽  
Fractional Excretion Of Sodium

The purpose of the present investigation was to study the effects of inhibition of monoamine oxidase (MAO) and/or catechol- O-methyltransferase (COMT), enzymes involved in the degradation of dopamine (DA) and serotonin (5-HT), on intrarenal DA and 5-HT, as reflected in the renal interstitial fluid (RIF) microdialysate and urine, and on renal function. Inhibition of MAO selectively increased RIF 5-HT from 3.16 ± 0.38 to 8.03 ± 1.83 pg/min ( n = 7, P < 0.05), concomitant with decreases in mean arterial blood pressure and glomerular filtration rate (2.09 ± 0.18 to 1.57 ± 0.22 ml/min, n = 7, P < 0.05). Inhibition of COMT significantly increased RIF DA (3.47 ± 0.70 to 8.68 ± 1.96 pg/min, n = 9, P < 0.05), urinary DA (2.00 ± 0.16 to 2.76 ± 0.26 ng/min, n = 9, P < 0.05), and absolute excretion of sodium (6.42 ± 2.00 to 9.82 ± 1.62 μmol/min, n = 10, P < 0.05). Combined inhibition of MAO and COMT significantly increased RIF DA, urinary DA, and urinary 5-HT, which was accompanied with increases in urine flow rate, and absolute (3.03 ± 0.59 to 8.40 ± 1.61 μmol/min, n = 9, P < 0.01) and fractional excretion of sodium. We conclude that inhibition of MAO selectively increases RIF 5-HT. COMT appears to be more important than MAO in the metabolism of intrarenal DA. Physiological increases in intrarenal DA/5-HT induced by inhibition of their degrading enzymes are accompanied with significant alterations of renal function.

Control of renal function during intrarenal infusion of endothelin

1990 ◽  
Vol 258 (5) ◽  
pp. F1232-F1236 ◽  
Author(s):  
D. L. Stacy ◽  
J. W. Scott ◽  
J. P. Granger
Keyword(s):  
Renal Function ◽  
Filtration Rate ◽  
Fractional Excretion ◽  
Systemic Arterial Pressure ◽  
Renal Hemodynamics ◽  
Direct Effects ◽  
Electrolyte Excretion ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium ◽  
Isolated Arteries

It has been demonstrated that bolus injections of a vasoconstrictor derived from endothelial cells, endothelin 1 (ET-1), constricts isolated arteries and increases blood pressure in animals when infused intravenously. The purpose of this study was to examine the direct effects of intrarenal infusions of ET-1 on renal function at doses that do not alter systemic arterial pressure. The effects of ET-1 on renal hemodynamics and electrolyte excretion were examined during 40 min of intrarenal infusions of ET-1 at rates of 1.15 and 5 ng.kg-1.min-1. Infusion of ET-1 (1.15 ng.kg-1.min-1) resulted in a transient increase in renal blood flow (RBF) followed by a progressive vasoconstriction, which reduced RBF by 23%. ET-1 decreased glomerular filtration rate (GFR) and had no significant effect on filtration fraction. Intrarenal infusion of ET-1 (1.15 ng.kg-1.min-1) had no effect on fractional excretion of sodium (FENa) or potassium. Infusion of ET-1 at a higher dose (5 ng.kg-1.min-1) produced further reductions in RBF, GFR, and FENa. These data indicate that ET-1 is a potent renal vasoconstrictor that could play a role in controlling renal hemodynamics.

Chronic effects of oral sulindac on renal haemodynamics and hormones in subjects with chronic renal disease

1986 ◽  
Vol 70 (3) ◽  
pp. 243-247 ◽  
Author(s):  
Charles P. Swainson ◽  
Peter Griffiths ◽  
Michael L. Watson
Keyword(s):  
Renal Function ◽  
Filtration Rate ◽  
Chronic Renal Disease ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Hormonal Control ◽  
Glomerular Function ◽  
Chronic Effects ◽  
Plasma Hormones

1. The effects of oral sulindac, 600 mg daily, on renal function and plasma hormones were studied in eight subjects with chronic renal failure. 2. Renal function and plasma hormones were measured before drug administration and then after taking sulindac for 28 days. 3. Effective renal plasma flow was reduced in all subjects after 28 days but the glomerular filtration rate did not change. 4. Plasma renin activity, potassium and aldosterone concentrations and urinary sodium excretion did not change but urinary prostaglandin E2 excretion fell significantly. 5. Sulindac may be a relatively renal-sparing drug in its effects on the hormonal control of glomerular function.

Renal and vascular effects of C-type and atrial natriuretic peptides in humans

1997 ◽  
Vol 273 (4) ◽  
pp. R1457-R1464 ◽  
Author(s):  
Isabelle Pham ◽  
Saïd Sediame ◽  
Geneviève Maistre ◽  
Françoise Roudot-Thoraval ◽  
Pierre-Etienne Chabrier ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Vascular Effects ◽  
Fractional Excretion Of Sodium ◽  
Endocrine Factor ◽  
Normal Men ◽  
Dose Dependent ◽  
Atrial Natriuretic

C-type natriuretic peptide (CNP) may affect renal and vascular functions differently from atrial natriuretic peptide (ANP). The objective of this study was to compare the renal and vascular actions of CNP to those of ANP in normal men. CNP or ANP (0.005, 0.01, and 0.05 μg ⋅ kg−1 ⋅ min−1) were given by infusion to eight healthy volunteers. CNP caused dose-dependent increases in natriuresis (UNa) and in the fractional excretion of sodium (FENa) with no effect on diuresis (UV), renal plasma flow, and glomerular filtration rate (GFR). Fraction of filtration (FF) increased only with the 0.05 μg ⋅ kg−1 ⋅ min−1CNP dose. ANP caused larger increases in UNa, FENa, and FF than CNP and also increased UV at 0.01 and 0.05 μg ⋅ kg−1 ⋅ min−1and GFR at 0.05 μg ⋅ kg−1 ⋅ min−1. Although the ANP and CNP infusions produced similar elevation in the respective peptides plasma levels, urinary and nephrogenous guanosine 3′,5′-cyclic monophosphate increased less in response to CNP than to ANP. Blood pressure, forearm blood flow, plasma renin activity, and aldosterone remained unaffected during the peptides infusion. Plasma ANP increased slightly during CNP infusion. Our data indicate a higher threshold of renal response to CNP than to ANP. In contrast to ANP, CNP probably may not act as an endocrine factor in humans.

Kidney cross transplants in Dahl salt-sensitive and salt-resistant rats

1992 ◽  
Vol 262 (6) ◽  
pp. H1809-H1817 ◽  
Author(s):  
P. C. Churchill ◽  
M. C. Churchill ◽  
A. K. Bidani
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Fractional Excretion ◽  
Transplanted Kidney ◽  
Native Kidney ◽  
Clearance Studies ◽  
Genetically Determined

Previous kidney cross-transplant studies have demonstrated that the genotype of the kidney plays a role in determining the blood pressure of the recipient in Dahl salt-sensitive (S) and salt-resistant (R) rats. The present studies were designed to elucidate this role. Kidney cross transplants were performed in unilaterally nephrectomized male recipients (John Rapp strains), such that each rat had a native kidney and a transplanted kidney of the opposite genotype. S and R rats with a native kidney and a transplanted kidney of the same genotype served as controls. After 4 wk on a 7.8% NaCl diet, rats were anesthetized and renal clearance studies were performed. S kidneys had lower glomerular filtration rate (GFR) and renal plasma flow (RPF) than R kidneys, and these differences were determined by the kidney's genotype rather than the recipient's, since S kidneys in R recipients tended to have lower GFR and RPF than R kidneys in S recipients. In contrast, independent of the kidney's genotype, the kidneys in S rats tended to have higher fractional excretion of H2O and Na (FEH2O and FENa) than the kidneys in R rats. Thus there were genetically determined differences in renal function between S and R rats; some (RPF and GFR) were intrinsic to the kidney, whereas others (FEH2O and FENa) were intrinsic to the host.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of endogenous endothelin on renal functions in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F34-F38
Author(s):  
K. Yamada ◽  
S. Yoshida
Keyword(s):  
Sodium Excretion ◽  
Salt Intake ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Sodium Balance ◽  
High Salt Intake ◽  
Fractional Excretion Of Sodium

This study was conducted to determine the involvement of endogenous endothelin (ET), a novel potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system by inhibiting ET action via infusion of a specific ET antiserum at a time of altered sodium balance. Infusion of 1:50 diluted ET antiserum, which completely inhibited renal vasoconstriction by the exogenously administered ET (0.25 to 1.0 nmol/kg), caused an increase in urinary sodium excretion and fractional excretion of sodium and a decrease in plasma renin concentration without significant changes in blood pressure, heart rate, glomerular filtration rate, renal plasma flow, and urine volume compared with the values with nonimmune serum in conscious rats fed a low-salt diet. A time control study showed no significant changes in all parameters. These results suggest that the state of low- compared to high-salt intake causes a relatively stronger activity of endogenous ET, and that the endogenous ET contributes to the adaptative modulations of sodium excretion via renal tubular action and renin release in association with the changed state of sodium balance.

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