Cardiorenal endocrine dynamics during volume expansion in hypothyroid dogs

1988 ◽  
Vol 255 (1) ◽  
pp. R61-R66 ◽  
Author(s):  
R. S. Zimmerman ◽  
J. Ryan ◽  
B. S. Edwards ◽  
G. Klee ◽  
D. Zimmerman ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Atrial Pressure ◽  
Endocrine Function ◽  
Hormonal Changes ◽  
Marked Rise ◽  
Excretory Function ◽  
Fractional Excretion Of Sodium

To address the role of atrial natriuretic factor (ANF) in hypothyroidism in the control of cardiorenal-endocrine function during volume loading, the relationships between atrial pressure, ANF, the renin-angiotensin-aldosterone system, and renal hemodynamic and excretory function were examined during and after acute 10% body wt saline volume infusion in pentobarbital-anesthetized hypothyroid dogs (n = 8). Hormonal changes before and after thyroidectomy were also evaluated. Four to 6 wk after thyroidectomy, ANF decreased and arginine vasopressin (AVP) and plasma renin activity (PRA) increased. Acute saline volume expansion caused an increase in ANF and decreases in AVP and PRA. Atrial pressure increased throughout volume expansion. Despite the absence of an increase in glomerular filtration rate (GFR) during volume expansion, urinary sodium excretion increased due to a marked rise in fractional excretion of sodium. These studies demonstrate that in hypothyroidism 1) ANF is decreased; 2) despite the decrease in basal ANF, increases in atrial pressure can stimulate relase of ANF; 3) despite the absence of an increase in GFR during volume expansion, fractional excretion of sodium increases associated with an increase in ANF; and 4) a lack of an increase in GFR during volume expansion is not related to an inability to increase ANF.

Cardiorenal-endocrine dynamics during and following volume expansion

1987 ◽  
Vol 252 (2) ◽  
pp. R336-R340 ◽  
Author(s):  
R. S. Zimmerman ◽  
B. S. Edwards ◽  
T. R. Schwab ◽  
D. M. Heublein ◽  
J. C. Burnett
Keyword(s):  
Body Weight ◽  
Volume Expansion ◽  
Volume Overload ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Excretory Function ◽  
Pulmonary Capillary ◽  
Anesthetized Dogs

The relationship between atrial pressure, atrial natriuretic peptide (ANP), the renin-angiotensin-aldosterone system, and renal hemodynamic and excretory function was examined during and following acute 10% body weight saline volume expansion and measurements were made at 3.3, 6.6, and 10% body weight volume expansion in pentobarbital anesthetized dogs (n = 10). Right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP), fractional excretion of Na (FENa), and ANP all increased in parallel during volume expansion. Plasma renin activity (PRA) and aldosterone decreased in parallel during 10% volume expansion. Following 10% volume expansion, saline was infused at the peak urine flow rate to maintain peak volume expansion. Despite continued saline infusion, RAP, PCWP, and ANP decreased in parallel. In contrast, FENa remained increased, and aldosterone and PRA remained depressed. These studies demonstrate that atrial pressures, ANP, and FENa increase in parallel during volume expansion; this suggests a role for ANP in modulating acute atrial volume overload. During stable volume expansion periods, however, despite a decrease in ANP levels, Na excretion remains elevated, suggesting that non-ANP mechanisms may be important in maintaining natriuresis during stable volume expansion.

Effect of intrarenal renin inhibition on renal hemodynamics and excretory function

1990 ◽  
Vol 259 (1) ◽  
pp. R7-R14 ◽  
Author(s):  
K. M. Verburg ◽  
J. R. Kadam ◽  
G. A. Young ◽  
S. H. Rosenberg ◽  
H. D. Kleinert
Keyword(s):  
Recovery Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Angiotensin System ◽  
Excretory Function ◽  
Fractional Excretion Of Sodium ◽  
Renin Inhibition

This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Intrarenal infusion of A-65317 (n = 6) at a dose of 0.01 micrograms.kg-1.min-1 elicited an increase (P less than 0.05) in renal blood flow (RBF) from 43.5 +/- 2.7 to 49.4 +/- 4.4 ml/min and glomerular filtration rate (GFR) from 6.3 +/- 0.3 to 6.9 +/- 0.4 ml/min, with no significant changes in mean arterial pressure (MAP) or plasma renin activity (PRA). Increases (P less than 0.05) in the urine flow rate (0.18 +/- 0.04 to 0.28 +/- 0.04 ml/min) and the fractional excretion of sodium (0.18 +/- 0.06 to 0.35 +/- 0.13%) were also observed. After a recovery period, the intrarenal infusion dose of A-65317 was increased to 0.1 microgram.kg-1.min-1 and RBF increased (P less than 0.05) from 42.9 +/- 3.9 to 53.0 +/- 3.7 ml/min in conjunction with a significant 85 +/- 4% inhibition of PRA and a 14 +/- 4 mmHg reduction in MAP. GFR and electrolyte excretion remained at control levels. Intrarenal infusion of vehicle (n = 6) had no significant effect on any of the variables studied. In a separate group of monkeys, intravenous (iv) infusion of A-65317 at 0.01 microgram.kg-1.min-1 (n = 5) did not result in significant changes from control.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

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.

Proximal tubule response in aldosterone escape

1989 ◽  
Vol 256 (1) ◽  
pp. R86-R90 ◽  
Author(s):  
J. M. Gonzalez-Campoy ◽  
J. Kachelski ◽  
J. C. Burnett ◽  
J. C. Romero ◽  
J. P. Granger ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Reabsorption ◽  
Hormonal Changes ◽  
Proximal Tubular ◽  
Temporal Profiles

The response of the proximal tubule to chronic aldosterone administration (15 micrograms.kg-1.day-1) was evaluated in eight conscious female mongrel dogs. Temporal profiles between hemodynamic and hormonal changes and the fractional excretions of sodium and lithium were established. Aldosterone infusion resulted in a significant decrease in urinary sodium excretion from 9.2 +/- 1.3 to 5.8 +/- 0.9 meq/h after 1 day, returning to normal by the 5th day. These changes in urinary sodium excretion were associated with significant elevations of the mean arterial pressure (MAP) from 105 +/- 5 to 111 +/- 6 mmHg and plasma atrial natriuretic factor concentrations (ANF) from 30 +/- 2 to 57 +/- 7 pg/ml beginning the 1st day of infusion. Plasma renin activity (PRA), on the other hand, was depressed by aldosterone, falling below the level of detectability. The fractional excretion of lithium increased significantly by day 2 of aldosterone infusion (from 29 +/- 3 to 44 +/- 6%), reflecting the proximal tubular response to the above changes. We conclude that the proximal tubule responds to increases in MAP and ANF and decreases in PRA during aldosterone infusion by decreasing sodium reabsorption. Subsequent nephron segments must also respond to the volume expansion produced by aldosterone, since the sustained proximal tubule natriuretic response is insufficient to explain all of escape.

Natriuretic Effect of Propranolol on Dogs with Chronic Bile-Duct Ligation

1978 ◽  
Vol 54 (6) ◽  
pp. 603-607 ◽  
Author(s):  
J. Winaver ◽  
C. Chaimovitz ◽  
O. S. Better
Keyword(s):  
Bile Duct ◽  
Volume Expansion ◽  
Bile Duct Ligation ◽  
Extracellular Volume ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Adrenergic Blockade ◽  
Duct Ligation ◽  
Fractional Excretion Of Sodium ◽  
Extracellular Volume Expansion

1. Chronic ligation of the bile duct in dogs is associated with salt retention and a blunted natriuretic response to extracellular volume expansion. The mechanism of this phenomenon has not been clarified. 2. We have examined the influence of chronic β-adrenergic blockade on sodium excretion in dogs with bile-duct ligation during extracellular hypotonic volume expansion. 3. Urinary excretion of sodium and fractional excretion of sodium rose significantly after 5 days of oral dl-propranolol administration to dogs with bile-duct ligation. 4. The antinatriuresis after bile-duct ligation was not followed by a significant alteration in the mean peripheral plasma renin activity as compared with control values. 5. It is suggested that propranolol can partially reverse the antinatriuresis of chronic bile-duct ligation, and that this is mediated by an extrarenal effect of the β-adrenergic blockade.

Role of renal interstitial hydrostatic pressure in natriuresis of systemic nitric oxide inhibition

1993 ◽  
Vol 264 (3) ◽  
pp. F411-F414 ◽  
Author(s):  
J. A. Haas ◽  
A. A. Khraibi ◽  
M. A. Perrella ◽  
F. G. Knox
Keyword(s):  
Nitric Oxide ◽  
Hydrostatic Pressure ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Significant Rise ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Suprarenal Aorta ◽  
Fractional Excretion Of Sodium

Systemic inhibition of nitric oxide synthesis with NG-monomethyl-L-arginine (L-NMMA) increases renal perfusion pressure (RPP) and urinary sodium excretion. Increased RPP has been proposed as one of the mechanisms for the natriuresis caused by intravenous infusion of L-NMMA. We tested the hypothesis that increases in renal interstitial hydrostatic pressure (RIHP) are required for the natriuresis of L-NMMA infusion. Experiments were performed in four groups of Sprague-Dawley rats in which partial aortic clamping and/or bilateral renal decapsulation was performed to control RPP and RIHP. Infusion of L-NMMA (15 mg/kg bolus + 500 micrograms.kg-1 x min-1 continuous infusion) increased RPP (delta+ 14 +/- 1 mmHg), RIHP (delta+ 3.6 +/- 0.7 mmHg), and fractional excretion of sodium (FENa; delta 2.4 +/- 0.6%, P < 0.005). When RPP was prevented from increasing by controlling RPP with an adjustable clamp around the suprarenal aorta, RIHP and FENa did not significantly change. When only RIHP was held constant by bilateral renal decapsulation, FENa was not significantly increased (delta+ 0.68 +/- 0.36%, not significant), despite a significant rise in RPP (delta+ 18 +/- 2 mmHg, P < 0.001). Control of both RPP and RIHP prevented the increase in FENa. Thus, when renal interstitial pressure was controlled, the infusion of L-NMMA did not result in an increase in FENa. These results demonstrate that an increase in RIHP is a necessary component in the natriuresis due to systemic infusion of L-NMMA.

ANF secretion and renal responses to volume expansion with equilibrated blood

1988 ◽  
Vol 255 (5) ◽  
pp. F936-F943 ◽  
Author(s):  
R. V. Paul ◽  
T. Ferguson ◽  
L. G. Navar
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
High Dose ◽  
Sprague Dawley ◽  
Blood Volume Expansion ◽  
Step Procedure ◽  
Sprague Dawley Rats ◽  
Fractional Excretion Of Sodium

To evaluate the role of atrial natriuretic factor (ANF) in the renal response to acute blood volume expansion without hemodilution, a reservoir syringe filled with donor rat blood was connected to the femoral artery and vein of anesthetized Sprague-Dawley rats to allow rapid equilibration of the reservoir with the intravascular blood. Volume expansion with blood from the reservoir in two steps (of 1 and 1.5% body wt, separated by 1 h, n = 5 rats) produced a mean peak increase in plasma immunoreactive ANF from 99 +/- 21 to 1,310 +/- 230 pg/ml (P less than 0.001); plasma ANF levels throughout these experiments correlated significantly with simultaneously measured urine flow (r = 0.74, P less than 0.005) and sodium excretion (r = 0.65, P less than 0.005). Another group (n = 7) underwent the same two-step procedure; after the second volume expansion, high-dose atriopeptin III infusion (0.4 microgram.kg-1.min-1 did not further increase fractional excretion of sodium (3.17 +/- 0.27 to 2.50 + 0.39%, P = NS). In another group (n = 9 rats), the same dose of atriopeptin III was started before any blood volume expansion. After the resulting hypotension was corrected by restoration of blood volume, an additional 1.5% body weight blood volume expansion did not further augment sodium excretion. We conclude that the diuresis and natriuresis, which occur in response to volume expansion without hemodilution, rise and fall in parallel with immunoreactive ANF in the plasma, and that ANF and acute blood volume expansion act on the kidney through a similar, saturable mechanism.

scholarly journals Acute hypoxia and endogenous renal endothelin.

1994 ◽  
Vol 4 (11) ◽  
pp. 1920-1924
Author(s):  
A Nir ◽  
A L Clavell ◽  
D Heublein ◽  
L L Aarhus ◽  
J C Burnett
Keyword(s):  
Acute Hypoxia ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Tissue ◽  
Control Group ◽  
Moderate Hypoxia ◽  
Time Control ◽  
Fractional Excretion Of Sodium ◽  
Air Ventilation ◽  
Hypoxic Group

Endothelin (ET) is a potent vasoconstrictor peptide of endothelial cell origin. Recent studies have suggested a nonvascular paracrine and/or autocrine role for endothelin in the kidney. This study was designed to elucidate the renal ET response to acute moderate hypoxia, as reflected by urinary ET excretory rate and renal tissue ET immunoreactivity, and to correlate these responses to the hemodynamic and excretory changes during hypoxia. Experiments were conducted in two groups of anesthetized dogs: hypoxic group (10% O2 ventilation: PO2, 44 mm Hg; N = 7) and time control group (room air ventilation: PO2, 111 mm Hg; N = 6). After 60 min of hypoxia or room air ventilation, kidneys were harvested and stained immunohistochemically for ET. Acute moderate hypoxia was associated with significant increases in urinary ET excretion, urine flow, urinary sodium excretion, and fractional excretion of sodium (P < 0.05). There was no significant change in GFR, RBF, renal vascular resistance, or mean arterial pressure. Renal immunohistochemistry for ET revealed increased staining in the proximal and distal tubules in the hypoxic group as compared with controls. This study demonstrates that acute moderate hypoxia results in increased urinary ET excretion and renal tubular ET immunoreactivity, in association with diuresis and natriuresis, and suggests a nonvascular role of endogenously produced renal ET in the regulation of sodium homeostasis during hypoxia.

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