Kaliuretic regulatory factors in the rat

1987 ◽  
Vol 253 (6) ◽  
pp. F1182-F1196 ◽  
Author(s):  
J. C. Rutledge ◽  
L. Rabinowitz
Keyword(s):  
Sodium Intake ◽  
Plasma Potassium ◽  
Urine Excretion ◽  
High Potassium ◽  
Regulatory Factors ◽  
Potassium Intake ◽  
Excretion Rates ◽  
Caloric Balance ◽  
Adrenalectomized Rats

To evaluate the role of aldosterone, plasma potassium, and sodium and urine excretion rates in controlling both total daily potassium excretion and the diurnal cyclic excretion of potassium, we performed experiments on unanesthetized, undisturbed rats kept in a 12-h light/12-h dark environment and fed a liquid diet. Independent variations were imposed on potassium intake, sodium intake, and, in groups of adrenalectomized rats, on aldosterone infusion rates. Potassium intake was 2.6, 10.6, and 18.7 meq/day. Sodium intake was 2.1, 6.7, and 17 meq/day. Aldosterone infusion was 0.1, 0.4, 1, and 10 times a basal rate of 1 microgram.day-1.100 g-1, with constant dexamethasone infusion at 1.43 micrograms.day-1.100 g-1. Twenty-four-hour excretion of potassium and sodium balanced 24-h intake of potassium and sodium regardless of the imposed combination of known regulatory factors. The amplitudes of potassium and sodium excretion during the diurnal cycle were each closely related to the ongoing levels of potassium and sodium intake. Plasma potassium was measured at the peak of the potassium cycle. It is suggested, based on analysis of the results, that when caloric balance was maintained, the amplitude of the diurnal potassium cycle was not importantly influenced by the rates of sodium and urine excretion, and, in addition to effects of aldosterone and plasma potassium concentration, the amplitude was importantly influenced by unspecified, homeostatically effective kaliuretic factors. Adrenalectomized rats receiving subbasal aldosterone replacement rejected the high potassium diet, were anuric, lost weight, and were severely hyperkalemic, observations indicating the necessity of adequate aldosterone for maintenance of potassium homeostasis.

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.

Diurnal potassium excretory cycles in the rat

1986 ◽  
Vol 250 (5) ◽  
pp. F930-F941 ◽  
Author(s):  
L. Rabinowitz ◽  
C. J. Wydner ◽  
K. M. Smith ◽  
H. Yamauchi
Keyword(s):  
Extracellular Fluid ◽  
Potassium Content ◽  
Extracellular Potassium ◽  
Dark Phase ◽  
Adrenal Steroids ◽  
Light Phase ◽  
High Potassium ◽  
Potassium Intake ◽  
Low Levels ◽  
Adrenalectomized Rats

Diurnal potassium cycles (DPC) were measured in unanesthetized undisturbed rats fed a liquid diet and maintained in a 12-h light-dark environment. A fourfold step increase in diet potassium content increased DPC amplitude without altering phase. After presentation of the high-potassium diet, the initial adaptive increase in excretion occurred within 1.5 h (diet given during dark phase) and within 6 h (diet given during light phase). On a day when food was withheld (no potassium intake), DPC were present but with a lowered amplitude. The amount of potassium excreted on a fasting day exceeded gut and extracellular fluid potassium content and was only modestly increased when rats were previously fed a high-potassium diet. In adrenalectomized rats that received no steroid replacement or received constant infusions of low levels of aldosterone, dexamethasone, or aldosterone plus dexamethasone, potassium balance and DPC were normal. It is concluded that the amplitude of DPC in the rat is determined in part by the availability of potassium from both intracellular and extracellular potassium pools; mechanisms independent of potassium intake can generate the DPC; and the presence or the cyclic secretion of adrenal steroids is not necessary for the generation of DPC in the rat.

Extrarenal potassium adaptation: role of skeletal muscle

1986 ◽  
Vol 251 (2) ◽  
pp. F313-F318 ◽  
Author(s):  
J. D. Blachley ◽  
B. P. Crider ◽  
J. H. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Binding Capacity ◽  
Lethal Dose ◽  
Plasma Potassium ◽  
Potassium Salts ◽  
Ouabain Binding ◽  
High Potassium ◽  
Potassium Adaptation

Following the ingestion of a high-potassium-content diet for only a few days, the plasma potassium of rats rises only modestly in response to a previously lethal dose of potassium salts. This acquired tolerance, termed potassium adaptation, is principally the result of increased capacity to excrete potassium into the urine. However, a substantial portion of the acute potassium dose is not immediately excreted and is apparently translocated into cells. Previous studies have failed to show an increase in the content of potassium of a variety of tissues from such animals. Using 86Rb as a potassium analogue, we have shown that the skeletal muscle of potassium-adapted rats takes up significantly greater amounts of potassium in vivo in response to an acute challenge than does that of control animals. Furthermore, the same animals exhibit greater efflux of 86Rb following the termination of the acute infusion. We have also shown that the Na+-K+-ATPase activity and ouabain-binding capacity of skeletal muscle microsomes are increased by the process of potassium adaptation. We conclude that skeletal muscle is an important participant in potassium adaptation and acts to temporarily buffer acute increases in the extracellular concentration of potassium.

Relationship between plasma potassium concentration and renal potassium excretion

1982 ◽  
Vol 242 (6) ◽  
pp. F599-F603 ◽  
Author(s):  
D. B. Young
Keyword(s):  
Renal Excretion ◽  
Potassium Concentration ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Potassium Intake ◽  
Arterial Ph ◽  
The Relationship ◽  
Renal Potassium Excretion

To study the relationship between extracellular potassium concentration and renal excretion of potassium, seven chronically adrenalectomized dogs were maintained on a constant intravenous infusion of aldosterone (50 micrograms/day), and constant sodium intake (30 meq/day ) while they received four levels of potassium intake--10, 30, 100, and 200 meq/day--for 7-10 days each. At the conclusion of each level of intake, plasma potassium and renal excretion as well as other variables known to influence potassium excretion were measured. There were minimal changes in arterial pH, mean arterial pressure, extracellular fluid volume, or glomerular filtration rate at any level of potassium intake. The values for plasma potassium and renal potassium excretion attained at each level of intake were: 3.13 +/- 0.24 and 10 +/- 2; 4.18 +/- 0.18 and 21 +/- 6; 4.31 +/- 0.11 and 66 +/- 10; and 4.75 +/- 0.10 meq/liter and 170 +/- 16 meq/day, respectively. Under these experimental conditions in which the levels of aldosterone, sodium intake, arterial pH, arterial pressure, extracellular fluid volume, and glomerular filtration rate remain constant, plasma potassium concentration appears to have a week effect on renal potassium excretion below the normal level of plasma potassium (approx. 11 meq/day change in excretion for each milliequivalent per liter change in concentration). Above the normal level, however, plasma potassium concentration has a powerful effect, 260 meq/day per milliequivalent per liter. The characteristics of the relationship between plasma potassium and renal potassium excretion make it ideally suited for controlling potassium excretion in response to greater than normal potassium intake.

The Antihypertensive Effect of Dietary Potassium Chloride Loading in Rats with Adrenal Regeneration Hypertension

1984 ◽  
Vol 66 (2) ◽  
pp. 129-140 ◽  
Author(s):  
K. E. Milmer ◽  
T. Bennett ◽  
S. M. Gardiner
Keyword(s):  
Antihypertensive Effect ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Nacl Solution ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Peripheral Vasodilatation ◽  
Male Wistar Rats ◽  
Potassium Loading

1. Adrenal regeneration hypertension was induced in male Wistar rats by unilateral adrenal enucleation, contralateral adrenalectomy and the provision of a 1% (w/v) NaCl solution for drinking. 2. A fivefold increase in dietary KCl content caused a significant reduction in the systolic blood pressure of hypertensive rats but not of control rats. 3. During the increase in potassium intake there was a marked polydipsia. When 1% NaCl solution was the drinking fluid, the resultant increase in sodium intake was associated with an abolition of the antihypertensive effect of potassium loading, but when the sodium intake was held constant, the antihypertensive effect was maintained. 4. In rats with adrenal regeneration hypertension, plasma volume was significantly higher, and packed cell volume and plasma protein concentrations were significantly lower than in control rats. These differences were abolished after 4 days of dietary KCl supplementation. 5. Increased dietary potassium intake was associated with significantly lower serum aldosterone concentrations and significantly higher plasma potassium concentrations in adrenal enucleated rats compared with controls. 6. The possibility that a reduction in extracellular fluid volume (due to a natriuresis) and/or a peripheral vasodilatation contributed to the antihypertensive effect of KCl loading is discussed.

scholarly journals Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake

2019 ◽  
Vol 30 (8) ◽  
pp. 1425-1438 ◽  
Author(s):  
Peng Wu ◽  
Zhong-Xiuzi Gao ◽  
Dan-Dan Zhang ◽  
Xiao-Tong Su ◽  
Wen-Hui Wang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Potassium Channel ◽  
Basolateral Membrane ◽  
Potassium Conductance ◽  
Plasma Potassium ◽  
Wild Type ◽  
High Potassium ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Low Potassium

BackgroundThe basolateral potassium channel in the distal convoluted tubule (DCT), comprising the inwardly rectifying potassium channel Kir4.1/Kir5.1 heterotetramer, plays a key role in mediating the effect of dietary potassium intake on the thiazide-sensitive NaCl cotransporter (NCC). The role of Kir5.1 (encoded by Kcnj16) in mediating effects of dietary potassium intake on the NCC and renal potassium excretion is unknown.MethodsWe used electrophysiology, renal clearance, and immunoblotting to study Kir4.1 in the DCT and NCC in Kir5.1 knockout (Kcnj16−/−) and wild-type (Kcnj16+/+) mice fed with normal, high, or low potassium diets.ResultsWe detected a 40-pS and 20-pS potassium channel in the basolateral membrane of the DCT in wild-type and knockout mice, respectively. Compared with wild-type, Kcnj16−/− mice fed a normal potassium diet had higher basolateral potassium conductance, a more negative DCT membrane potential, higher expression of phosphorylated NCC (pNCC) and total NCC (tNCC), and augmented thiazide-induced natriuresis. Neither high- nor low-potassium diets affected the basolateral DCT’s potassium conductance and membrane potential in Kcnj16−/− mice. Although high potassium reduced and low potassium increased the expression of pNCC and tNCC in wild-type mice, these effects were absent in Kcnj16−/− mice. High potassium intake inhibited and low intake augmented thiazide-induced natriuresis in wild-type but not in Kcnj16−/− mice. Compared with wild-type, Kcnj16−/− mice with normal potassium intake had slightly lower plasma potassium but were more hyperkalemic with prolonged high potassium intake and more hypokalemic during potassium restriction.ConclusionsKir5.1 is essential for dietary potassium’s effect on NCC and for maintaining potassium homeostasis.

scholarly journals Role of COX-2-derived metabolites in regulation of the renal hemodynamic response to norepinephrine

2001 ◽  
Vol 281 (5) ◽  
pp. F975-F982 ◽  
Author(s):  
Maria T. Llinás ◽  
Ruth López ◽  
Francisca Rodríguez ◽  
Francisco Roig ◽  
F. Javier Salazar
Keyword(s):  
Sodium Intake ◽  
Hemodynamic Response ◽  
Hemodynamic Effects ◽  
Relative Contribution ◽  
Low Sodium ◽  
Renal Hemodynamic ◽  
Cox Inhibitor ◽  
Cox 2 ◽  
Excretion Rates

The objective of this study was to examine the role of cylcooxygenase (COX)-2-derived prostaglandins (PG) in modulating the renal hemodynamic effects of norepinephrine (NE) during low or normal sodium intake. The relative contribution of each COX isoform in producing the PG that attenuate the renal NE effects during normal sodium intake was also evaluated. The renal response to three doses of NE (50, 100, and 250 ng · kg−1 · min−1) was evaluated in anesthetized dogs pretreated with vehicle, a selective COX-2 inhibitor (nimesulide), or a nonselective COX inhibitor (meclofenamate). Intrarenal infusion of the two lower doses of NE in vehicle-pretreated dogs with normal sodium intake ( n = 8) elicited an increase in renal vascular resistance (RVR; 21 and 34%) without inducing changes in glomerular filtration rate (GFR). The highest dose of NE in this group induced a further increment in RVR (113%) and a decrease in GFR (33%). Pretreatment with nimesulide in dogs with normal sodium intake ( n = 7) did not modify the NE-induced increments in RVR but enhanced the decreases in GFR induced by the three NE doses (12, 26, and 64%). The renal hemodynamic response to NE in meclofenamate-pretreated dogs with normal sodium intake ( n = 7) was similar to that found in dogs pretreated with nimesulide. Infusion of the lowest dose of NE to vehicle-pretreated dogs with low sodium intake ( n = 6) did not modify GFR and elicited an increase in RVR (42%). Infusion of the second and third doses of NE led to a decrease in GFR (35 and 91%) and a rise in RVR (82 and 587%). Infusion of the first two doses of NE in nimesulide-pretreated dogs with low sodium intake ( n= 5) induced a fall in GFR (64 and 92%) and an increase in RVR (174 and 2,293%) that were greater ( P < 0.05) than those induced by NE in vehicle-pretreated dogs. The elevation in the urinary excretion rates of PGE2 and 6-keto-PGF1α elicited by NE was prevented in the nimesulide-pretreated dogs. Our results show that COX-2 inhibition potentiates the renal hemodynamic effects of NE and propose that the PG involved in modulating them are mainly derived from COX-2 activity.

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats

2001 ◽  
Vol 281 (3) ◽  
pp. R723-R729 ◽  
Author(s):  
G. H. M. Schoorlemmer ◽  
A. K. Johnson ◽  
R. L. Thunhorst
Keyword(s):  
Intravenous Infusion ◽  
Sodium Intake ◽  
Peripheral Circulation ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
Brain Ventricle ◽  
The Brain ◽  
Adrenalectomized Rats

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 ± 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 ± 12% ( n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10–15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.

ALTERATIONS OF ALDOSTERONE BIOSYNTHESIS BY RAT ADRENAL TISSUE DUE TO INCREASED INTAKE OF SODIUM AND POTASSIUM

1968 ◽  
Vol 58 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Jürg Müller
Keyword(s):  
Adrenal Glands ◽  
Sodium Intake ◽  
Potassium Ions ◽  
High Potassium ◽  
High Sodium ◽  
Potassium Intake ◽  
High Sodium Intake ◽  
Test Conditions ◽  
Sodium And Potassium

ABSTRACT Three groups of rats received respectively the following drinking fluids for two weeks: sucrose 5%; NaCl 0.154 m + sucrose; KCl 0.154 m+ sucrose. Aldosterone biosynthesis by quartered adrenal glands of these animals was studied under various in vitro conditions. Adrenals from rats drinking sucrose alone produced significantly more aldosterone under all conditions of incubation than adrenals from rats drinking NaCl, which produced more corticosterone and deoxycorticosterone. Tissue from animals drinking NaCl converted less unlabelled progesterone, 11β-hydroxyprogesterone, deoxycorticosterone and corticosterone to aldosterone and incorporated less tritiated pregnenolone, progesterone, deoxycorticosterone and corticosterone into aldosterone. Adrenals from rats drinking KCl produced less aldosterone than adrenals from rats drinking sucrose under basal conditions but not under stimulation by ACTH or potassium ions. In both groups, the production of corticosterone and of deoxycorticosterone was the same under various test conditions. These results indicate that a high sodium intake inactivates one or both enzymes essential for the conversion of corticosterone to aldosterone, whereas a high potassium intake has no significant effect on these later steps of aldosterone biosynthesis.

scholarly journals Diminished Antiproteinuric Effect Of The Angiotensin Receptor Blocker Losartan During High Potassium Intake In Patients With Ckd

2021 ◽  
Author(s):  
Rosa D Wouda ◽  
Femke Waanders ◽  
Dick de Zeeuw ◽  
Gerjan Navis ◽  
Liffert Vogt ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Angiotensin Receptor Blockers ◽  
Dietary Sodium ◽  
Angiotensin Receptor ◽  
High Potassium ◽  
Potassium Intake ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Urinary Potassium

Abstract Background Angiotensin receptor blockers (ARBs) lower blood pressure (BP) and proteinuria and reduce renal disease progression in many—but not all—patients. Reduction of dietary sodium intake improves these effects of ARBs. Dietary potassium intake affects BP and proteinuria. We set out to address the effect of potassium intake on BP and proteinuria response to losartan in non-diabetic proteinuric chronic kidney disease (CKD) patients. Methods We performed a post-hoc analysis of a placebo-controlled interventional cross-over study in 33 non-diabetic proteinuric patients (baseline mean arterial pressure and proteinuria: 105 mmHg and 3.8 g/d, respectively). Patients were treated for 6 weeks with placebo, losartan, and losartan/hydrochlorothiazide, combined with a habitual (∼200 mmol/d) and low-sodium diet (&lt;100 mmol/d), in randomized order. To analyze the effects of potassium intake, we categorized patients based on median split of 24 h urinary potassium excretion, reflecting potassium intake. Results Mean potassium intake was stable during all 6 treatment periods. Losartan and losartan/hydrochlorothiazide lowered BP and proteinuria in all treatment groups. Patients with high potassium intake showed no difference in the BP effects compared to patients with low potassium intake. The antiproteinuric response to losartan monotherapy and losartan combined with hydrochlorothiazide during the habitual sodium diet was significantly diminished in patients with high potassium intake (20% vs. 41%, p = 0.011 and 48% vs 64%, p = 0.036). These differences in antiproteinuric response abolished when shifting to the low sodium diet. Conclusions In proteinuric CKD patients, the proteinuria, but not BP-lowering response to losartan during a habitual high sodium diet was hampered during high potassium intake. Differences disappeared after sodium status change by low-sodium diet.

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