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

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.

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Effect of high-dose fentanyl on renal function in dogs

Sao Paulo Medical Journal ◽

10.1590/s1516-31801997000300006 ◽

1997 ◽

Vol 115 (3) ◽

pp. 1433-1439 ◽

Cited By ~ 3

Author(s):

Yara Marcondes Machado Castiglia ◽

José Reinaldo Cerqueira Braz ◽

Pedro Thadeu Galvão Vianna ◽

Lino Lemonica ◽

Luiz Antonio Vane

Keyword(s):

Renal Function ◽

Extracellular Volume ◽

Fractional Excretion ◽

Blood Collection ◽

High Dose ◽

Sodium Pentobarbital ◽

Fluid Infusion ◽

Fractional Excretion Of Sodium ◽

Left Femoral Artery ◽

Extracellular Volume Expansion

Our objective was to determine the effects of high-dose fentanyl on canine renal function (RF). We anesthetized with sodium pentobarbital (SP) 16 dogs, randomly divided into 2 groups: in G1, SP was given alone, and in G2, combined with 0.05 mg.kg-1 fentanyl. All animals were ventilated artificially and had catheterized left and right femoral veins and left femoral artery for fluid infusion, drug administration, blood collection, and hemodynamic measurement. Urine was collected throughout the experiment. Attributes of RF were studied. SP did not alter RF, which was significantly altered by fentanyl. In G2, slower heart rates, mean arterial pressure, creatinine clearance, urinary output, osmolar clearance and fractional excretion of sodium and potassium were observed. G1 had a behavior attributed to extracellular volume expansion and no RF alterations. In G2, we observed significant decreases in RF due to opioid-induced hemodynamic changes, not discarding the possible action of aldosterone.

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Antiphosphaturic action of 25 (OH) vitamin D3 in experimental Fanconi syndrome.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1979.236.2.e90 ◽

1979 ◽

Vol 236 (2) ◽

pp. E90

Author(s):

M M Popovtzer ◽

S K Mehandru ◽

D Saghafi ◽

M S Blum

Keyword(s):

Parathyroid Hormone ◽

Urinary Excretion ◽

Vitamin D3 ◽

Volume Expansion ◽

Fanconi Syndrome ◽

Extracellular Volume ◽

Fractional Excretion ◽

Renal Handling ◽

Phosphate Depletion ◽

Extracellular Volume Expansion

Renal handling of phosphorus was studied in the following groups of parathyroidectomized rats with maleate-induced Fanconi syndrome: 1) 6 rats receiving intravenous parathyroid hormone, 2) 6 rats receiving intravenous dibutyryl cyclic AMP (DBcAMP), 3) 6 rats undergoing volume expansion with saline, 4) 12 rats receiving intravenous 25 (OH)vitamin D3, 5) 12 rats with acute hypercalcemia induced by intravenous CaCl2, 6) 6 rats with phosphate deprivation, and 7) 6 rats receiving intravenous calcitonin. Parathyroid hormone and calcitonin failed to increase the urinary excretion of both cAMP and phosphorus. Likewise, DBcAMP failed to increase the urinary excretion of phosphorus. Extracellular volume expansion and hypercalcemia (serum calcium 12.9 +/- 0.7 mg/100 ml) did not alter the tubular reabsorption of phosphorus. In phosphate-deprived animals, the fractional excretion 0.16 +/- 0.05 (mean +/- SE) was lower than that in the control animals (maleate-treated without phosphate depletion), 0.46 +/- 0.04 (P less than 0.001). 25 (OH)vitamin D3 decreased the fractional excretion of phosphorus from 0.39 +/- 0.03 in the control (maleate-treated not receiving 25 (OH)vitamin D3) to 0.23 +/- 0.02 (P less than 0.001) in the experimental animals. The present study demonstrated an antiphosphaturic effect of 25(OH)vitamin D3 in experimental Fanconi syndrome; the mechanism of this action is not well understood.

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Haemodynamic and renal evolution of the bile duct-ligated rat

Clinical Science ◽

10.1042/cs0980611 ◽

2000 ◽

Vol 98 (5) ◽

pp. 611-617 ◽

Cited By ~ 12

Author(s):

Concepción MARTÍNEZ-PRIETO ◽

M. Clara ORTÍZ ◽

Lourdes A. FORTEPIANI ◽

Jose Antonio RUIZ-MACIÁ ◽

Noemí M. ATUCHA ◽

...

Keyword(s):

Portal Hypertension ◽

Bile Duct ◽

Rat Model ◽

Bile Duct Ligation ◽

Plasma Renin ◽

Sodium Balance ◽

Sodium Retention ◽

Peripheral Vasodilation ◽

Duct Ligation ◽

Conscious Animals

In the present study we have characterized the evolution of changes in systemic haemodynamics (thermodilution in conscious animals) and sodium balance (metabolic cages) in a model of liver cirrhosis induced by chronic bile duct ligation (BDL). Mean arterial pressure (BDL, 111.5±4.7 mmHg; sham-operated, 122.9±3.0 mmHg) and peripheral vascular resistance (BDL, 2.63±0.08 units; sham-operated, 2.93±0.09 units) were lower in BDL rats from day 12 after surgery and decreased progressively throughout the following days. Portal hypertension was evident earlier in BDL rats and was maintained throughout the study period. Cardiac index (BDL, 58.8±3.9 ml·min-1·100 g-1; sham-operated, 43.9±1.5 ml·min-1·100 g-1) and stroke volume (BDL, 147.2±12.7 ml·beat-1·100 g-1; sham-operated, 109.0±4.2 ml·beat-1·100 g-1) were significantly elevated in the BDL rats only from day 18 after surgery. There were no significant differences in sodium balance between the groups until day 16 after surgery, at which time BDL animals started to retain significantly more sodium than the controls. Sodium retention increased progressively, and at day 20 BDL rats had retained 0.7 mmol/100 g more than the control animals (accumulated retention: BDL, 2.2±0.2 mmol/100 g; sham-operated, 1.5±0.2 mmol/100 g). Plasma renin activity and aldosterone concentration were not elevated in the BDL animals at days 12, 16 or 20 after surgery. These data indicate that the BDL rat model shows early portal hypertension, peripheral vasodilation and arterial hypotension, several days before sodium retention is detectable, and in the absence of changes in plasma levels of renin and aldosterone. Overall, these data suggest that, in the BDL rat model, sodium retention is secondary to portal hypertension and peripheral vasodilation.

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Mechanism of decrease in plasma renin activity during volume expansion

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.6.1550 ◽

1976 ◽

Vol 230 (6) ◽

pp. 1550-1554 ◽

Cited By ~ 9

Author(s):

SO Stitzer ◽

M Martinez-Maldonado

Keyword(s):

Plasma Renin Activity ◽

Volume Expansion ◽

Extracellular Volume ◽

Plasma Renin ◽

Renin Activity ◽

Present Experimental Condition ◽

A Value ◽

Group I ◽

Extracellular Volume Expansion ◽

Filtered Load

The importance of filtered load of sodium and extracellular volume expansion (ECVE( per se on plasma renin activity (PRA) was studied in two groups of hydropenic dogs. Group I protocol consisted of bilateral ureteral obstruction (UO) followed by isotonic ECVE and finally UO release. During UO, PRA rose significantly above control (15.4 leads to 41.7 ng/ml per h). Superimposition of ECVE did not significantly alter PRA, but UO release returned PRA toward control (24.8 ng/ml per h). Fractional sodium excretion (FE(Na)) after UO release was higher than control (0.6 leads to 12.6%). In group II, ECVE preceded UO and caused a fall in PRA below control (16.8 leads to 4.8 ng/ml per h). FE(Na) was significantly increased over control (0.3 leads to 14.7%). Superimposition of UO reversed the fall in PRA to a value not significantly different from control. On release of UO PRA fell, but not significantly, whereas FE(Na) fell to 12.6%, a value not different from that during ECVE alone. The results indicate that filtration is required for ECVE to elicit a fall in PRA, under the present experimental condition.

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Renal Phosphate Adaptation in Uraemic Dogs with a Remnant Kidney

Clinical Science ◽

10.1042/cs0600273 ◽

1981 ◽

Vol 60 (3) ◽

pp. 273-282 ◽

Cited By ~ 8

Author(s):

S.-F. Wen ◽

R. W. Stoll

Keyword(s):

Renal Failure ◽

Parathyroid Hormone ◽

Chronic Renal Failure ◽

Volume Expansion ◽

Extracellular Volume ◽

Fractional Excretion ◽

Phosphate Transport ◽

Extracellular Volume Expansion ◽

Fractional Excretion Of Phosphate ◽

Remnant Kidney

1. Clearance and micropuncture studies were performed in 27 dogs made uraemic by segmental infarction to examine the factors responsible for phosphate adaptation in chronic renal failure. 2. The animals were studied before and after extracellular volume expansion to 10% of body weight in the presence and absence of parathyroid glands. The results were compared with 19 normal dogs studied under similar experimental conditions. 3. In the dogs with a remnant kidney and intact parathyroids adaptation of phosphate transport was evident, with a high fractional excretion of phosphate. Thyroparathyroidectomy 3 days before study in the dogs with a remnant kidney and moderate renal failure reduced fractional excretion of phosphate to near normal values, indicating a major role of parathyroid hormone in phosphate adaptation. Extracellular volume expansion in these thyroparathyroidectomized uraemic dogs led to an exaggerated phosphaturic response with fractional excretion of phosphate returning towards the value in the uraemic dogs with intact parathyroid glands. Thus acute extracellular volume expansion could also contribute to the increase in fractional phosphate excretion, but extracellular volume probably plays a relatively minor role in the adaptation of phosphate excretion. 4. With more advanced renal failure fractional excretion of phosphate remained high, even after thyroparathyroidectomy, indicating that parathyroid hormone-independent factors become important for phosphate adaptation in the advanced stage of renal failure. The nature of parathyroid hormone-independent changes in fractional phosphate reabsorption in chronic renal failure remains unknown. 5. Proximal tubular fluid/plasma ultrafiltrate phosphate ratios were high in all groups of dogs with a remnant kidney regardless of thyroparathyroidectomy or the degree of renal failure. The non-specific nature of the proximal tubule pattern of phosphate transport indicates that phosphate adaptation is primarily determined by alterations in phosphate transport at a site distal to the proximal convoluted tubule. Alternatively, deep nephrons may play a greater role in determination of the overall phosphate adaptation in the chronically diseased kidney.

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The kidney and cardiovascular system in obstructive jaundice: Functional and metabolic studies in conscious rats

Clinical Science ◽

10.1042/cs0730593 ◽

1987 ◽

Vol 73 (6) ◽

pp. 593-599 ◽

Cited By ~ 11

Author(s):

Stefan Heidenreich ◽

Erich Brinkema ◽

Andreas Martin ◽

Rainer Düsing ◽

Jochen Kipnowski ◽

...

Keyword(s):

Bile Duct ◽

Mitochondrial Function ◽

Fractional Excretion ◽

Kidney Cortex ◽

Aortic Tissue ◽

Metabolic Disturbances ◽

Duct Ligation ◽

Fractional Excretion Of Sodium ◽

Pg E2

1. The effects of jaundice on renal and circulatory function were investigated in chronic bile duct ligated (CBDL). rats 6 days after surgery. Sham operated (SO) animals served as controls. 2. Body weight was significantly reduced, whereas blood pressure remained unaltered, 6 days after bile duct ligation when serum bilirubin had risen to 169 ± 18 (SEM) as compared with 2.8 ± 0.3 μmol/l in SO rats. When compared with control values before surgery, urinary volume had significantly increased and absolute excretion of sodium, potassium, chloride and phosphate had decreased on day 6 after CBDL. Endogenous creatinine clearance was markedly depressed when compared with SO rats. Whereas fractional excretion of potassium remained unaltered, fractional excretion of sodium and of phosphate was significantly increased. 3. Except for a significant increase in urinary thromboxane B2 (TXB2) excretion in CBDL rats, no significant changes were observed in urinary excretion of prostaglandin (PG) E2, in the synthesis of PGE2, 6-keto-PGF1α and TXB2 by isolated aortic tissue in vitro, nor in renal and cardiac adenosine triphosphatase activities or renal cortical mitochondrial function. 4. The adenosine triphosphate content of kidney cortex and cardiac mitochondrial function were significantly depressed in CBDL rats. 5. The results demonstrate that jaundice in CBDL rats is associated with functional and metabolic disturbances of the kidney and cardiac muscle, which may contribute to the renal and haemodynamic characteristics observed in jaundiced animals and humans.

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Cardiorenal endocrine dynamics during volume expansion in hypothyroid dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.255.1.r61 ◽

1988 ◽

Vol 255 (1) ◽

pp. R61-R66 ◽

Cited By ~ 5

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.

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