A vasopressin-mediated diminution of potassium excretion in water-loaded man

1985 ◽  
Vol 69 (5) ◽  
pp. 601-606 ◽  
Author(s):  
J. Buckley ◽  
E. M. Gebruers ◽  
W. J. Hall ◽  
N. M. B. Harrington
Keyword(s):  
Urine Osmolality ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Specific Effects ◽  
Antidiuretic Effect ◽  
Endogenous Prostaglandins ◽  
Potassium Absorption ◽  
Prior Administration

1. Intravenous vasopressin (1–3 μ-units min−1 kg−1) had an antidiuretic effect on water-loaded man and also diminished potassium excretion. As noted by others, aspirin (2.4 g) enhanced the antidiuretic effect of vasopressin, but the fall in potassium excretion was not modified by prior administration of aspirin, which makes it unlikely that the fall was due to the release of endogenous prostaglandins. 2. After terminating the infusion of vasopressin, the fall in potassium output persisted longer than the antidiuresis, which makes it unlikely that the antikaliuretic effect of vasopressin is secondary to its effect on urine flow. 3. The unchanged antikaliuretic effect of vasopressin after aspirin treatment, together with its persistence after terminating the infusion, suggest the possible existence of vasopressin-mediated potassium absorption in the distal nephron in certain circumstances. 4. Aspirin administration had specific effects of its own in water-loaded man. It decreased both the water diuresis and sodium excretion but did not alter potassium excretion or urine osmolality.

Antidiuretic effect of perorally administered DDAVP in hydrated humans

1984 ◽  
Vol 105 (4) ◽  
pp. 474-476 ◽  
Author(s):  
Hans Vilhardt ◽  
Peter Bie
Keyword(s):  
Drinking Water ◽  
Body Weight ◽  
Intestinal Mucosa ◽  
Arginine Vasopressin ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Concomitant Increase ◽  
Water Diuresis ◽  
Antidiuretic Effect ◽  
Dose Dependent

Abstract. Urine volume and osmolality were measured in volunteers hydrated with drinking water (2% of body weight). During maintained water diuresis DDAVP (1-deamino-8-D-arginine vasopressin) dissolved in water was administered per os. Within 15-30 min a dose-dependent antidiuretic response occurred with a concomitant increase in urine osmolality. Administration of DDAVP through a duodenal tube caused similar antidiuretic effects indicating that the intact peptide can be absorbed from the intestinal mucosa.

The Role of Vasopressin and Urea in the Renal Concentrating Defect of Patients with Cirrhosis of the Liver

1971 ◽  
Vol 41 (5) ◽  
pp. 441-452 ◽  
Author(s):  
C. A. Vaamonde ◽  
Liliana S. Vaamonde ◽  
J. I. Presser ◽  
H. J. Morosi ◽  
E. L. Klingler ◽  
...  
Keyword(s):  
Urine Osmolality ◽  
Urine Flow ◽  
Cirrhosis Of The Liver ◽  
Urinary Concentration ◽  
Renal Tubules ◽  
Urea Synthesis ◽  
Water Diuresis ◽  
Flow Rates ◽  
Cirrhotic Patients ◽  
Concentrating Defect

1. The maximal urine osmolality in response to vasopressin during water diuresis and during hydropenia was studied in twenty patients with cirrhosis and sixteen noncirrhotic subjects under controlled dietary conditions. 2. The cirrhotic patients exhibited a significantly lower maximal urine osmolality under both experimental conditions. 3. During water diuresis decompensated and compensated cirrhotics had comparable maximal urine osmolalities after vasopressin. A decreased response of the renal tubules to vasopressin does not appear to have a significant role in the concentrating defect. 4. The cirrhotic patients had a significantly lower excretion rate of urea at high (water diuresis) and low (vasopressin antidiuresis or hydropenia) urine flow rates. The lower urine urea concentration accounted for most of the decrease observed in maximal urinary concentration. After vasopressin administration the absolute tubular reabsorption of urea was also significantly lower in cirrhotic patients. The results suggest that a decrease in the medullary urea content decreases medullary osmolality resulting in the defect in urine concentration noted in these cirrhotic patients at low urine flow rates. 5. Protein depletion or decreased urea synthesis may in part be responsible for the decreased availability of urea for the concentrating process in cirrhosis. 6. Lack of correlation between concentrating and diluting capacity in these patients suggested that decreased delivery of sodium to the distal site might not be the limiting factor common to both renal functional abnormalities observed in cirrhosis of the liver.

Urine and papilla concentrations during transition from hypotonic to hypertonic urine

1965 ◽  
Vol 208 (2) ◽  
pp. 397-400 ◽  
Author(s):  
H. L. White ◽  
Doris Rolf
Keyword(s):  
Urine Osmolality ◽  
Sodium Concentration ◽  
Significant Rise ◽  
Urine Flow ◽  
Water Diuresis ◽  
Osmotic Equilibration

Dogs in water diuresis, with high urine flow and low urine osmolality and sodium concentration, had papilla fluid osmolality of 398 milliosmols/kg H2O and papilla fluid sodium concentration of 116 millimolal. At 5.5 min after laparotomy and 100 mU of vasopressin intravenously, papilla fluid osmolality and sodium concentration showed no significant rise, but urine osmolality and sodium concentration had risen greatly. At longer intervals, up to 13 min, papilla osmolality rose to above 600 mM with a further rise in urine osmolality; osmotic equilibration between urine and papilla fluid was attained at about 10 min Papilla fluid sodium concentration rose after 5.5 min Cortex fluid remained isosmolal with plasma.

Role of vasopressin in maintenance of potassium homeostasis in severe hemorrhage

2013 ◽  
Vol 305 (2) ◽  
pp. R101-R103 ◽  
Author(s):  
Catherine F. T. Uyehara ◽  
Joy Sarkar
Keyword(s):  
Sharp Increase ◽  
Plasma Potassium ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Volume Loss ◽  
Distal Nephron ◽  
Potassium Homeostasis ◽  
Normal Limits ◽  
Severe Hemorrhage

Uncontrolled elevation in plasma potassium within minutes of rapid blood volume loss is associated with mortality and distinguishes nonsurvivors of severe hemorrhage from survivors. In a pig model of severe hemorrhage, we discovered that along with a sharp increase in plasma potassium coincident with a shut down of urine flow, nonsurvivors also had an insufficient vasopressin response to hemorrhage. In contrast, survivors did have elevated vasopressin levels in response to hemorrhage and maintained plasma potassium within normal limits. While it has been demonstrated for some time that vasopressin can influence secretion of potassium in the distal nephron, the magnitude of this effect and conditions under which this contributes to physiological modulation of potassium excretion has yet to be defined. In this review, we assess the evidence that would suggest that vasopressin plays a key role in modulating potassium excretion and is important in the regulation of potassium homeostasis during hemorrhage.

Potassium and sodium excretion and potassium homeostasis during acute hypokalemia

1965 ◽  
Vol 208 (6) ◽  
pp. 1143-1152 ◽  
Author(s):  
Robert R. Siegel ◽  
William D. Lotspeich
Keyword(s):  
Sodium Excretion ◽  
Extracellular Fluid ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Close Coupling ◽  
Potassium Homeostasis ◽  
Blood Ph ◽  
Total Body

Decreased potassium and increased sodium excretion were observed in dogs acutely potassium-depleted by hemodialysis. Potassium excretion at constant blood pH varied directly with plasma [K+]. When filtered Na load and urine flow were constant during K+ depletion, increase in Na excretion was equivalent to decrease in K+ excretion, suggesting close coupling between transtubular movements of the two ions. Large changes in plasma [K+] (30%) and K+ excretion (50%) were produced with removal of a relatively small amount (estimated 3%) of total body K+. Plasma [K+] decrease during depletion was rapidly decelerated by movement of intracellular K+ into the extracellular fluid (ECF). When ECF [K+] stabilized, further decrease in K+ excretion ceased despite continued reduction of total body K+. It appears: 1) that tubular secretion of K+ is directly and rapidly responsive to reduction in ECF [K+]; 2) that low ECF [K+] may simultaneously impair contraluminal K+ uptake and Na extrusion, reducing K+ excretion and Na reabsorption during acute hypokalemia. Stoichiometry of changes suggests a 1:1 coupling between K+ secretion and moiety of Na reabsorption in the distal nephron.

Induction of water diuresis by endothelin in rats

1992 ◽  
Vol 263 (3) ◽  
pp. F516-F526 ◽  
Author(s):  
J. Schnermann ◽  
J. N. Lorenz ◽  
J. P. Briggs ◽  
J. A. Keiser
Keyword(s):  
Produced Water ◽  
Enzyme Inhibitor ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Water Diuresis ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Vasopressin Secretion ◽  
Induced Changes

Experiments were performed in anesthetized rats to examine the possibility that endothelin (ET) modifies renal epithelial function in addition to its well-established hemodynamic actions. Infusion of ET-3 at rates between 34 and 178 ng.kg-1.min-1 was in many cases followed by a rise in urine flow and a persistent decrease in urine osmolality, whereas glomerular filtration rate (GFR) did not significantly change. The extent of ET-induced diuresis was dependent on the response of GFR: in rats in which ET-3 infusion caused a marked reduction of GFR (greater than 70%) ET-induced diuresis was not seen, even though urine osmolality still fell significantly. From animal to animal, ET-induced changes of urine flow or GFR did not correlate significantly with the rate of ET-3 infusion. ET-1, another ET isopeptide, also produced water diuresis when administered in GFR-neutral doses. Urinary excretion of total solutes and of sodium was not significantly altered by ET-3. Infusion of vasopressin blunted the diuretic effect of ET-3, whereas ET-3-induced water diuresis was not measurably altered by chronic or acute treatment with a converting enzyme inhibitor or by acute inhibition of prostaglandin synthesis. Induction of water diuresis was not secondary to an inhibition of vasopressin secretion since it could be demonstrated in homozygous Brattleboro rats in which antidiuresis was produced by the infusion of vasopressin at a rate of 200 microU.kg-1.min-1. These data suggest that ET may be an inhibitory modulator of the hydrosmotic action of vasopressin at the level of the renal collecting duct.

EFFECTS OF ARGININE-, LYSINE- AND LEUCINE-VASOPRESSIN ON URINARY OSMOLALITY AND RATE OF URINE FLOW IN HYDRATED RATS AND DOGS

1959 ◽  
Vol XXXII (I) ◽  
pp. 134-141 ◽  
Author(s):  
Niels A. Thorn
Keyword(s):  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
The Other ◽  
Maximum Increase ◽  
Urinary Osmolality ◽  
Lysine Vasopressin

ABSTRACT Arginine-, lysine- and leucine-vasopressin, injected i. v. into hydrated rats or dogs caused different patterns of response in that urine osmolality fell much more slowly after the maximum increase following arginine-vasopressin, than after the other two preparations. Using 3 different parameters for antidiuretic response, arginine-vasopressin was somewhat more potent than leucine-vasopressin in both rats and dogs, considerably more potent than lysine-vasopressin in rats, and much more so in dogs.

Homeostatic potassium excretion in fed and fasted sheep

1988 ◽  
Vol 254 (2) ◽  
pp. R357-R380 ◽  
Author(s):  
L. Rabinowitz ◽  
D. M. Green ◽  
R. L. Sarason ◽  
H. Yamauchi
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Urine Flow Rate ◽  
Potassium Excretion ◽  
Adult Sheep ◽  
Blood Ph ◽  
Low Levels ◽  
K Concentration ◽  
Filtered Load

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

Effects of sodium intake on steady-state potassium excretion

1984 ◽  
Vol 246 (6) ◽  
pp. F772-F778 ◽  
Author(s):  
D. B. Young ◽  
T. E. Jackson ◽  
U. Tipayamontri ◽  
R. C. Scott
Keyword(s):  
Steady State ◽  
Potassium Concentration ◽  
Sodium Intake ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Concentration Data ◽  
Potassium Intake ◽  
Independent Variable ◽  
The Relationship

The effects of changes in sodium intake on the steady-state relationship between plasma potassium concentration and potassium excretion were studied in 15 chronically adrenalectomized dogs. Throughout the experiments the dogs received aldosterone at a rate of 50 micrograms/day and methylprednisolone at 1 mg/day. The relationship between plasma potassium and steady-state potassium excretion was obtained by changing potassium intake from 10 to 30 to 100 meq/day, each level being maintained for 7-10 days. At the conclusion of each period at a given level of potassium intake, plasma potassium and excretion were measured and plotted, plasma potassium being the independent variable. Such a relationship was obtained while the dogs were on three different levels of sodium intake: 10, 100, and 200 meq/day. The curves from the data obtained at 100 and 200 meq/day sodium intake both were shifted to the left of the curve obtained at 10 meq/day (P less than 0.05), although the 100 and 200 meq/day curves were not different from each other. On the basis of these data one could predict that, at a plasma potassium concentration of 4.0 meq/liter, the animals would excrete potassium at a rate of 17 meq/day on a 10 meq/day sodium intake, 37 meq/day on a 100 meq/day sodium intake, and 47 meq/day on a 200 meq/day sodium intake. Urine flow and electrolyte concentration data are consistent with the hypothesis that the sodium intake effect on potassium excretion was mediated through increases in distal nephron flow rate and decreases in distal nephron potassium concentration.

Familial hypothalamic diabetes insipidus in rats (Brattleboro strain)

1964 ◽  
Vol 206 (2) ◽  
pp. 425-430 ◽  
Author(s):  
H. Valtin ◽  
H. A. Schroeder
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Supraoptic Nucleus ◽  
Spontaneous Mutation ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Neurosecretory Material ◽  
Carrier Protein ◽  
Marked Diminution ◽  
Long Evans

Familial hypothalamic diabetes insipidus ( DI) has arisen as an apparently spontaneous mutation from a strain of Long-Evans hooded rats being bred for unrelated researches not involving radioactivity. The DI rats decrease water intake and urine flow, and increase urine osmolality in response to injected vasopressin. They concentrate their urines only minimally or not at all in response to dehydration, hypertonic saline, nicotine, or stress, and their serum osmolalities and sodium concentrations are significantly higher than those of normal animals. They show marked diminution of neurosecretory material in the neurohypophysis and supraoptic nucleus. The data suggest that the deficiency causing DI in these rats is a lack or dearth of synthesis of vasopressin or its carrier protein, or both.

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