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.

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.

Aldosterone is a physiologically significant kaliuretic hormone

1987 ◽  
Vol 252 (6) ◽  
pp. F1048-F1054
Author(s):  
W. R. Adam ◽  
A. G. Ellis ◽  
B. A. Adams
Keyword(s):  
Plasma Potassium ◽  
Sodium Content ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Potassium Excretion ◽  
Sodium Potassium ◽  
Creatinine Excretion ◽  
Dietary Potassium ◽  
Food Load

To study the role of aldosterone in the short-term control of potassium excretion, rats were gavaged with a liquid diet containing 10-20% of their daily caloric and potassium intake, with a range of sodium intakes. Levels of (effective) aldosterone at the time of gavage were manipulated by administration of spironolactone, aldosterone, and adrenalectomy. Urinary sodium, potassium, and creatinine excretion were measured in conscious unrestrained rats for 2 h after the food load, and then blood was collected for measurement of plasma potassium, aldosterone, and renin activity. Potassium excretion was dependent on both dietary potassium and a minimum dietary sodium content. Potassium excretion was reduced by spironolactone and adrenalectomy and increased by acute aldosterone treatment in most dietary groups. These results strongly suggest that the ambient levels of aldosterone are important in determining potassium excretion following food ingestion. Plasma aldosterone was higher with the higher potassium and lower sodium content diets. Changes in plasma aldosterone, with variations in dietary potassium or sodium, suggest a role for aldosterone in subsequent potassium excretion.

Role of distal delivery of filtrate in impaired renal dilution of the hypothyroid rat

1976 ◽  
Vol 230 (3) ◽  
pp. 699-705 ◽  
Author(s):  
UF Michael ◽  
J Kelley ◽  
H Alpert ◽  
CA Vaamonde
Keyword(s):  
Free Water ◽  
Urine Flow ◽  
Distal Nephron ◽  
Sprague Dawley ◽  
Diluting Segment ◽  
Free Water Clearance ◽  
Sprague Dawley Rats ◽  
And Control ◽  
Distal Delivery

Free water clearance (CH2O) was measured during hypotonic saline infusion in Sprague-Dawley and in Brattleboro (DI) rats with 131I-induced hypothyroidism and their age-matched controls. At peak urine flow, which was similar in hypothyroid DI (HDI) and control DI (CDI) rats, inulin clearance (CIn/kg) and CH2O/kg were 23 and 20% (P less than 0.02) lower in HDI. Fractional urine flow and fractional sodium excretion were 30 and 40% (P less than 0.001) higher in HDI. Utilization of distal delivery of filtrate for CH2O, formation was 16% less in HDI (P less than 0.01). Papillary osmolality was not higher in HDI rats. Data in Sprague-Dawley rats were similar to those of the DI rats, indicating that endogenous ADH was effectively suppressed. It is concluded: 1) delivery of filtrate out of the proximal tubule was not diminished in hypothyroid rats in spite of a decrease in CIn; 2) despite a similar delivery of filtrate to the distal diluting site, CH2O formation was less in hypothyroid rats than in controls; 3) these data suggest that a defect in the diluting segment could be unmasked at high rates of filtrate delivered to the distal nephron; 4) this defect could be either due to impaired sodium chloride reabsorption or due to increased backdiffusion of water in the distal nephron.

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.

Renal response of newborn dog to potassium loading

1986 ◽  
Vol 251 (3) ◽  
pp. F513-F519 ◽  
Author(s):  
J. M. Lorenz ◽  
L. I. Kleinman ◽  
T. A. Disney
Keyword(s):  
Filtration Rate ◽  
Potassium Concentration ◽  
Excretion Rate ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Renal Response ◽  
Loaded State ◽  
Potassium Secretion ◽  
Potassium Loading

The renal response to potassium loading was studied in 14 newborn (6-20 days of age) and 14 adult mongrel dogs in order to determine the capacity of the newborn to excrete potassium load. Eight newborn and eight adult dogs were infused with 20 mueq of potassium chloride X min-1 X kg body wt-1 for 240 min. Adults excreted a significantly greater proportion of the potassium load during the 240-min infusion than did newborns (72 +/- 4 vs. 52 +/- 4%, P = 0.003). The infusion resulted in a significantly greater increase in plasma potassium concentration in the newborn (3.9 +/- 0.3 meq/liter) than in the adult (2.8 +/- 0.4 meq/liter), P = 0.05. Average potassium excretion rate per body weight was greater in the adult than newborn during potassium loading (15.0 +/- 1.0 vs. 10.4 +/- 0.7 mu eq X min-1. kg body wt-1, P = 0.003); however, average potassium excretion corrected for glomerular filtration rate was not significantly different between the adult and newborn (3.2 +/- 0.2 vs. 3.0 +/- 0.2 mu eq/ml filtered, P greater than 0.20). In another six newborn and six adult dogs, blockade of distal nephron potassium secretion with amiloride in the potassium-loaded state inhibited more than 90% of potassium excretion in both the newborn and adult.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The role of the BK channel in potassium homeostasis and flow-induced renal potassium excretion

2007 ◽  
Vol 72 (5) ◽  
pp. 566-573 ◽  
Author(s):  
T. Rieg ◽  
V. Vallon ◽  
M. Sausbier ◽  
U. Sausbier ◽  
B. Kaissling ◽  
...  
Keyword(s):  
Bk Channel ◽  
Potassium Excretion ◽  
Potassium Homeostasis ◽  
Renal Potassium Excretion

World Economic Crisis as a Process of Substitution of Technological Modes

2009 ◽  
pp. 26-38 ◽  
Author(s):  
S. Glaziev
Keyword(s):  
Economic Crisis ◽  
Economic Activity ◽  
Sharp Increase ◽  
Energy Resources ◽  
Long Wave ◽  
The World ◽  
World Economic ◽  
Technological Mode ◽  
World Economic Crisis

The article analyzes fundamental reasons for the world economic crisis in the light of global technological shifts. It proves that it is caused by the substitution of technological modes. It is shown that sharp increase and slump in stock indices and prices for energy resources are typical of the process of technological substitution which occurs regularly according to the rhythm of long-wave fluctuations of the world economic activity. The article rationalizes a package of anti-crisis measures aimed at stimulating the new technological mode. Its structure and role of the locomotive factor of the new long wave of economic growth are revealed.

The Renal Outer Medullary Potassium Channel (ROMK): An Intriguing Pharmacological Target for an Innovative Class of Diuretic Drugs

2018 ◽  
Vol 25 (23) ◽  
pp. 2627-2636 ◽  
Author(s):  
Vincenzo Calderone ◽  
Alma Martelli ◽  
Eugenia Piragine ◽  
Valentina Citi ◽  
Lara Testai ◽  
...  
Keyword(s):  
Physiological Role ◽  
Clinical Use ◽  
Diuretic Activity ◽  
First Line ◽  
Potassium Homeostasis ◽  
Diuretic Drugs ◽  
Pharmacological Target ◽  
Diuretic Agents ◽  
Effective Drugs

In the last four decades, the several classes of diuretics, currently available for clinical use, have been the first line option for the therapy of widespread cardiovascular and non-cardiovascular diseases. Diuretic drugs generally exhibit an overall favourable risk/benefit balance. However, they are not devoid of side effects. In particular, all the classes of diuretics cause alteration of potassium homeostasis. <p> In recent years, understanding of the physiological role of the renal outer medullary potassium (ROMK) channels, has shown an intriguing pharmacological target for developing an innovative class of diuretic agents: the ROMK inhibitors. This novel class is expected to promote diuretic activity comparable to (or even higher than) that provided by the most effective drugs used in clinics (such as furosemide), with limited effects on potassium homeostasis. <p> In this review, the physio-pharmacological roles of ROMK channels in the renal function are reported, along with the most representative molecules which have been currently developed as ROMK inhibitors.

scholarly journals With-No-Lysine Kinase 1 (WNK1) Augments TRPV4 Function in the Aldosterone-Sensitive Distal Nephron

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1482
Author(s):  
Viktor N. Tomilin ◽  
Kyrylo Pyrshev ◽  
Naghmeh Hassanzadeh Khayyat ◽  
Oleg Zaika ◽  
Oleh Pochynyuk
Keyword(s):  
Collecting Duct ◽  
Chinese Hamster ◽  
Dominant Negative ◽  
K Channel ◽  
Apical Plasma Membrane ◽  
Dependent Manner ◽  
Distal Nephron ◽  
Potassium Homeostasis ◽  
Wnk Kinases ◽  
K Secretion

Kidneys play a central role in regulation of potassium homeostasis and maintenance of plasma K+ levels within a narrow physiological range. With-no-lysine (WNK) kinases, specifically WNK1 and WNK4, have been recognized to regulate K+ balance, in part, by orchestrating maxi K+ channel (BK)-dependent K+ secretion in the aldosterone-sensitive distal nephron (ASDN), which includes the connecting tubule and collecting duct. We recently demonstrated that the Ca2+-permeable TRPV4 channel is essential for BK activation in the ASDN. Furthermore, high K+ diet increases TRPV4 activity and expression largely in an aldosterone-dependent manner. In the current study, we aimed to test whether WNK kinases contribute to regulation of TRPV4 activity and its stimulation by aldosterone. Systemic inhibition of WNK with WNK463 (1 mg/kgBW for 3 days) markedly decreased TRPV4-dependent Ca2+ influx in freshly isolated split-opened collecting ducts. Aldosterone greatly increased TRPV4 activity and expression in cultured mpkCCDc14 cells and this effect was abolished in the presence of WNK463. Selective inhibition of WNK1 with WNK-in-11 (400 nM, 24 h) recapitulated the effects of WNK463 on TRPV4-dependent Ca2+ influx. Interestingly, WNK-in-11 did not interfere with up-regulation of TRPV4 expression by aldosterone, but prevented translocation of the channel to the apical plasma membrane. Furthermore, co-expression of TRPV4 and WNK1 into Chinese hamster ovary (CHO) cells increased the macroscopic TRPV4-dependent cation currents. In contrast, over-expression of TRPV4 with a dominant negative WNK1 variant (K233M) decreased the whole-cell currents, suggesting both stimulatory and permissive roles of WNK1 in regulation of TRPV4 activity. Overall, we show that WNK1 is essential for setting functional TRPV4 expression in the ASDN at the baseline and in response to aldosterone. We propose that this new mechanism contributes to regulation of K+ secretion and, by extension, urinary K+ levels to maintain systemic potassium homeostasis.

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