Further Evidence in Vivo for a Circulating Natriuretic Substance after Expanding the Blood Volume in Rats

1980 ◽  
Vol 59 (6) ◽  
pp. 423-433 ◽  
Author(s):  
Catherine A. Knock
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Significant Rise ◽  
Urinary Sodium ◽  
Bilateral Nephrectomy ◽  
Experimental Protocol ◽  
Equivalent Time

1. The blood volume of 18 rats was expanded with blood with which they were equilibrated. In another 18 rats undergoing the same experimental protocol, the blood volume was not expanded. 2. In some rats the urine was reinfused. 3. A 1 ml portion of plasma obtained either 1 h after the blood volume was expanded, or at an equivalent time from the control rats, was injected intravenously into an assay rat. 4. The injection of plasma produced a gradual and significant rise in sodium excretion in the assay rat when it was obtained from an animal with an expanded blood volume, the urine of which was being reinfused. 5. When the increase in blood volume was sustained by a preceding bilateral nephrectomy, instead of urine reinfusion, the injection of 1 ml of plasma into an assay rat did not cause a rise in urinary sodium excretion. 6. It is concluded that the natriuresis involved in the assay rat was caused by a natriuretic substance in the 1 ml of plasma obtained from the blood-volume-expanded urine-reinfused rat. 7. The experiments suggest that the natriuretic substance is excreted in the urine and may be produced in the kidney.

Evidence in Vivo for a Circulating Natriuretic Substance in Rats after Expanding the Blood Volume

1980 ◽  
Vol 59 (6) ◽  
pp. 411-421 ◽  
Author(s):  
Catherine A. Knock ◽  
H. E. De Wardener
Keyword(s):  
Blood Transfusion ◽  
Blood Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
The Other ◽  
Not Given ◽  
The Cross ◽  
The Difference

1. Five rats were volume expanded by infusing a volume of blood equivalent to one-third of the estimated blood volume. In six control experiments the same transfusion was given without expanding the blood volume, as an equal volume of blood was simultaneously removed. Sodium excretion increased significantly more after the blood volume was expanded than in the control experiments. 2. Pairs of rats placed on opposite scale pans of a trip balance were cross-circulated by means of arteriovenous bypasses. The blood volume of the rats could be kept constant by keeping the balance in equilibrium. 3. One of each pair of rats received a blood transfusion which either did or did not expand its blood volume. Sodium excretion was measured in the transfused rat and in the recipient rat, the blood volume of which was kept constant. 4. Sodium excretion in the six recipient rats cross-circulated with rats with an expanded blood volume was not significantly different from that in six recipient rats, cross-circulated with rats given a transfusion which did not expand the blood volume. 5. The cross-circulation experiments were repeated, with the difference that the urine of the transfused rat was reinfused. Under these conditions, sodium excretion in 11 recipient rats cross-circulated with blood volume expanded rats was significantly greater than in eight recipient rats cross-circulated with rats given a transfusion which did not expand the blood volume. 6. In cross-circulation experiments in which a blood transfusion was not given urine reinfusion of one rat did not affect sodium excretion of the other rat. 7. It is concluded that the rise in urinary sodium excretion which occurs in an isovolaemic recipient rat cross-circulated with a urine reinfused rat with an expanded blood volume is due to a change in the concentration of a circulating substance.

The Effect of Expanding the Blood Volume of a Dog on the Short-Circuit Current across an Isolated Frog Skin Incorporated in the Dog's Circulation

1970 ◽  
Vol 38 (6) ◽  
pp. 629-648 ◽  
Author(s):  
D. M. Nutbourne ◽  
J. D. Howse ◽  
R. W. Schrier ◽  
L. B. Talner ◽  
M. G. Ventom ◽  
...  
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Blood Circulation ◽  
Frog Skin ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
The Other ◽  
Active Sodium

1. A frog skin was incorporated into the blood circulation of a dog. Each side of the skin was supplied with blood at a constant temperature, flow and pressure. 2. In the experiments in which the blood volume of the dog was expanded with equilibrated blood, there was a fall in the short-circuit current across all eight frog skins. The fall in current began 10 min after the start of the transfusion and reached its lowest value 15–30 min after the end of the transfusion. The dog showed a simultaneous rise in urinary sodium excretion. 3. In the experiments in which the blood volume was not expanded, there was no change in the trend in the short-circuit current in five of the eight skins. There was a fall in current across the other three skins; the pattern of this fall differed from that which occurred when the blood volume was expanded. There was no rise in the rate of urinary sodium excretion in any of the dogs. 4. It is concluded that when a dog's blood volume is expanded the dog alters the concentration of some circulating substance, and that this change causes a fall in the rate of active sodium transport across the frog skin.

The Effect of Brain Extracts on Urinary Sodium Excretion of the Rat and the Intracellular Sodium Concentration of Renal Tubule Fragments

1974 ◽  
Vol 47 (3) ◽  
pp. 201-213 ◽  
Author(s):  
E. M. Clarkson ◽  
K. G. Koutsaimanis ◽  
M. Davidman ◽  
M. Du Bois ◽  
W. P. Penn ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Gel Filtration ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Significant Rise ◽  
Intracellular Sodium ◽  
Urinary Sodium ◽  
Conscious Rat ◽  
Intracellular Sodium Concentration ◽  
Brain Extracts

1. Extracts were prepared from bovine hypothalamus and cerebral cortex by gel filtration on Sephadex G-25 and G-50. 2. The vasopressin in the hypothalamic extracts was inactivated with thioglycollate and the effectiveness of inactivation was tested in the alcohol-anaesthetized rat. 3. The inactivated hypothalamic extracts caused a significant rise, and the cortical extracts an insignificant fall, in the urinary sodium excretion of the conscious rat. 4. Incubation of tubule fragments in hypothalamic extracts caused a significant rise in intracellular sodium concentration of the tubules when compared with incubation in Ringer, whereas incubation in cortical extracts caused a rise which was not significant. Nevertheless the rise in intracellular sodium concentration produced by incubating the tubules in hypothalamic extracts was not significantly different from the rise produced by incubation in cortical extracts.

Atrial natriuretic peptide: Physiological release associated with natriuresis during water immersion in man

1986 ◽  
Vol 71 (3) ◽  
pp. 319-322 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Millar ◽  
J. P. O'Hare ◽  
J. C. MacKenzie ◽  
R. J. M. Corrall ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Natriuretic Hormone ◽  
The Mean ◽  
Atrial Natriuretic

1. Thermoneutral water immersion produces a physiological increase of thoracic blood volume, raises central venous pressure and increases urinary sodium excretion by a hitherto ill-understood mechanism. We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). 2. During water immersion there was a highly significant (P < 0.001) twofold increase of the mean plasma ANP concentration and a doubling of the mean urinary sodium excretion. Both were unchanged during the control experiments. 3. These results are consistent with the hypotheses (a) that ANP is released into plasma in response to central blood volume expansion and (b) that it functions as a natriuretic hormone in normal man under physiological conditions.

Multiple, random spot urine sampling for estimating urinary sodium excretion

2021 ◽  
Author(s):  
Gianluigi Ardissino ◽  
Antonio Vergori ◽  
Cesare Vergori ◽  
Laura Martelli ◽  
Valeria Daccò ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Spot Urine ◽  
Urine Sampling

scholarly journals Association between 24-h urinary sodium and potassium excretion and blood pressure among Chinese adults aged 18–69 years

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Inverse Association ◽  
Potassium Excretion ◽  
Chinese Adults ◽  
Potassium Intake ◽  
Sodium And Potassium

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.

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