Effects of Aprotinin on Renal Function and Urinary Prostaglandin Excretion in Conscious Rats after Acute Salt Loading

1979 ◽  
Vol 56 (6) ◽  
pp. 547-553 ◽  
Author(s):  
H. J. Kramer ◽  
T. Moch ◽  
L. Von Sicherer ◽  
R. Düsing
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Prostaglandin E2 ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Salt Loading ◽  
Expansion Phase ◽  
Conscious Rats

1. Aprotinin, a potent kallikrein inhibitor, was given to conscious rats with and without expansion of the extracellular fluid volume with isotonic saline. 2. In noa-expanded rats aprotinin had no effect on arterial pressure, glomerular filtration rate (GFR), hippuran clearance, urinary flow rate, absolute sodium and potassium excretion or free-water clearance. 3. In volume-expanded rats aprotinin significantly reduced GFR, hippuran clearance, urine volume (V) UNaV, UKV and Cwater/GFR without effect on systemic arterial pressure. 4. Urinary immunoreactive prostaglandin E2 excretion significantly increased during the expansion phase but returned to below the control range during stable extracellular fluid volume expansion. 5. Aprotinin significantly suppressed urinary immunoreactive prostaglandin E2 excretion in non-expanded rats and in volume-expanded rats during the expansion phase, but not during stable expansion. 6. The results suggest that the kallikrein-kinin system may contribute to changes in renal function during extracellular volume expansion. This action may not necessarily be associated with changes in renal prostaglandin E2 activity.

RENAL RESPONSE TO INFUSION OF ISOTONIC RINGER-LOCKE SOLUTION: EFFECT OF HYPOPHYSECTOMY

1977 ◽  
Vol 74 (2) ◽  
pp. 193-204
Author(s):  
J. T. BAKER ◽  
S. SOLOMON
Keyword(s):  
Body Weight ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Water Reabsorption ◽  
Locke Solution ◽  
Hypophysectomized Rats ◽  
Distal Tubules

A comparison of the renal response to extracellular fluid volume expansion (5% body weight) was made between 25 normal and 25 chronically hypophysectomized rats. The extracellular fluid compartments averaged 25 ± 1% of body weight in both groups during control, fasted conditions. Extracellular fluid volume increased to 33 ± 1% in hypophysectomized and 34 ± 2% in normal rats during expansion, based on body weight. In addition, filtration fraction was similar in both normal and hypophysectomized rats during control (0·29 ± 0·03 and 0·26 ± 0·02 respectively) and infusion of Ringer–Locke solution (0·24 ± 0·05 and 0·27 ± 0·05 respectively). Thus our results cannot be explained by differences in the degree of expansion or failure to increase filtration in proportion to plasma flow. During infusion of isotonic Ringer–Locke solution, fractional water and sodium excretion both averaged 5·1% in normal rats and only 1·3% and 0·82% respectively in hypophysectomized rats. The ratio of single nephron to whole kidney filtration rate failed to increase as much in hypophysectomized compared with normal rats. Significant increases of fractional volume excretion occurred in both groups by the end of the accessible portion of the proximal tubule. However, fractional water reabsorption was depressed significantly more in normal (mean = 37%) than in hypophysectomized rats (mean = 19%). Fractional water reabsorption in distal tubules was similar in both groups during expansion. Arterial pressure was lower in hypophysectomized rats under control conditions, but showed similar changes during expansion compared with normal rats. Passage time decreased significantly in all groups after Ringer–Locke infusion, but remained prolonged in hypophysectomized rats in proximal and distal tubules. It is concluded that chronic hypophysectomy results in a less efficient renal excretion of volume and sodium chloride load. This inefficiency appears to be related in part to (1) failure of the proximal tubule to depress water reabsorption to a level equivalent to normal rats, and (2) failure to re-distribute flow to outer cortical glomeruli following extracellular fluid volume expansion in hypophysectomized rats.

Extravascular lung water after extracellular fluid volume expansion in dogs

1977 ◽  
Vol 42 (4) ◽  
pp. 624-629 ◽  
Author(s):  
P. D. Snashall ◽  
W. J. Weidner ◽  
N. C. Staub
Keyword(s):  
Extravascular Lung Water ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Weight Ratio ◽  
Dry Weight ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Lung Water ◽  
Lung Weight ◽  
Extracellular Fluid Volume Expansion

We have compared extravascular lung water after extracellular fluid volume expansion with that predicted from lung sucrose space measured in control dogs. In control lungs mean extravascular water:dry weight ratio was 3.81 +/- 0.16 (SD) (n = 5) and extravascular sucrose space/dry weight was 1.79 +/- 0.45 (n = 4). After acute expansion of extracellular fluid volume by 10% of body weight mean extravascular water:dry lung weight was 4.17 +/- 0.27 (m = 5), less than half the predicted increase to 4.63 +/- 0.19, suggesting some degree of protection. After 20% (n = 4), 30% (n = 2), and 40% (n = 1) expansion, no protection was demonstrated and there was considerable scatter of lung water at each infusion volume. When volume expansion increased pulmonary capillary intravascular forces (due to decreased protein osmotic pressure and increased hydrostatic pressure) by more than 20 cmH2O there was a linear increase in extravascular lung water with increasing intravascular forces. Three dogs did not conform to this relationship and had disproportionately large increases in lung water, possibly due to alveolar flooding.

scholarly journals On the mechanism of the phosphaturia of extracellular fluid volume expansion in the dog

1973 ◽  
Vol 3 (4) ◽  
pp. 230-237 ◽  
Author(s):  
Liliana Gradowska ◽  
Sali Caglar ◽  
Ernest Rutherford ◽  
Herschel Harter ◽  
Eduardo Slatopolsky
Keyword(s):  
Volume Expansion ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Extracellular Fluid Volume Expansion

Role of renal arterial pressure in the regulation of extracellular volume in conscious dogs

1992 ◽  
Vol 82 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Gabriele Kaczmarczyk ◽  
Klaus Schröder ◽  
Dirk Lampe ◽  
Rainer Mohnhaupt
Keyword(s):  
Body Weight ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Central Venous ◽  
Infusion Period

1. This study in conscious dogs examined the quantitative effects of a reduction in the renal arterial pressure on the renal homoeostatic responses to an acute extracellular fluid volume expansion. 2. Seven female beagle dogs were chronically instrumented with two aortic catheters, one central venous catheter and a suprarenal aortic cuff, and were kept under standardized conditions on a constant high dietary sodium intake (14.5 mmol of Na+ day−1 kg−1 body weight). 3. After a 60 min control period, 0.9% (w/v) NaCl was infused at a rate of 1 ml min−1 kg−1 body weight for 60 min (infusion period). Two different protocols were applied during the infusion period: renal arterial pressure was maintained at 102 ± 1 mmHg by means of a servo-feedback control circuit (RAP-sc, 14 experiments) or was left free (RAP-f, 14 experiments). 4. During the infusion period, in the RAP-sc protocol as well as in the RAP-f protocol, the mean arterial pressure increased by 10 mmHg, the heart rate increased by 20 beats/min, the central venous pressure increased by 4 cmH2O and the glomerular filtration rate (control 5.1 ± 0.3 ml min−1 kg−1 body weight, mean ± sem) increased by 1 ml min−1 kg−1. 5. Plasma renin activity [control 0.85 ± 0.15 (RAP-f) and 1.08 ± 0.23 (RAP-sc) pmol of angiotensin I h−1 ml−1] decreased similarly in both protocols. 6. Renal sodium excretion, fractional sodium excretion and urine volume increased more in the RAP-f experiments than in the RAP-sc experiments (P<0.05), renal sodium excretion from 8.2 to 70.1 (RAP-f) and from 7.7 to 47.4 (RAP-sc) μmol min−1 kg−1 body weight, fractional sodium excretion from 1.1 to 8.0 (RAP-f) and from 1.0 to 5.4 (RAP-sc)% and urine volume from 39 to 586 (RAP-f) and from 38 to 471 (RAP-sc) μl min−1 kg−1 body weight. 7. In the RAP-f experiments as well as in the RAP-sc experiments, urinary sodium excretion increased with expansion of the extracellular fluid volume, which increased by a maximum of 21% (fasting extracellular fluid volume: 206 ± 4 ml/kg body weight, six dogs, 28 days). 8. The increase in renal arterial pressure contributed significantly to the renal homoeostatic response, as 21% less urine and 31% less sodium were excreted when the extracellular fluid volume was expanded and the renal arterial pressure was kept constant below control pressure rather than being allowed to rise. The differences in sodium and water excretion were mainly due to the effect of renal arterial pressure on tubular reabsorption. However, the striking increase in sodium and urine excretion which occurred despite the reduction in renal arterial pressure emphasizes the importance of other homoeostatic factors involved in body fluid regulation.

scholarly journals On the influence of extracellular fluid volume expansion on bicarbonate reabsorption in the rat

1969 ◽  
Vol 48 (9) ◽  
pp. 1754-1760 ◽  
Author(s):  
Mabel L. Purkerson ◽  
Herbert Lubowitz ◽  
Rose W. White ◽  
Neal S. Bricker
Keyword(s):  
Volume Expansion ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Bicarbonate Reabsorption ◽  
Extracellular Fluid Volume Expansion

scholarly journals Role of parathyroid hormone in the phosphaturia of extracellular fluid volume expansion

1975 ◽  
Vol 7 (5) ◽  
pp. 317-324 ◽  
Author(s):  
Edward G. Schneider ◽  
Ralph S. Goldsmith ◽  
Claud D. Arnaud ◽  
Franklin G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Extracellular Fluid Volume Expansion
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