SOME EFFECTS OF DIETARY POTASSIUM UPON DIGESTIBILITY, SERUM ELECTROLYTES AND UTILIZATION OF POTASSIUM, SODIUM, NITROGEN AND WATER IN HEIFERS

1967 ◽  
Vol 47 (1) ◽  
pp. 39-46 ◽  
Author(s):  
V. V. E. St. Omer ◽  
W. K. Roberts

Balance studies were conducted with heifers weighing between 210–258 kg to determine effects of different dietary potassium levels, 156.6 (low), 439.4 (medium) and 1,086.8 (high) meq upon nutrient utilization. The low potassium ration produced an average negative potassium balance of 25.2 meq daily, while the other rations produced positive potassium balances. Urinary potassium excretion was markedly affected by potassium level while fecal potassium excretion was much less affected: in general, the higher the potassium intake, the higher the urinary and fecal potassium excretions. All heifers were in positive sodium balance and dietary level of potassium did not significantly influence either urinary or fecal excretion of sodium. Nitrogen balance was not significantly affected by treatment, but urinary ammonia excretion was significantly (P < 0.01) higher when the low potassium ration was fed. Water consumption and urine volume were significantly (P < 0.01) higher for the heifers fed high potassium, but water balance was not affected. Apparent digestibilities of energy, dry matter, nitrogen, crude fiber and ether extract were not significantly affected by treatment.Serum potassium levels were lower (P < 0.05) and phosphorus higher (P < 0.05) in heifers receiving the low than in heifers receiving the high level of potassium. Serum concentrations of sodium, chloride, calcium and magnesium were not significantly affected by dietary potassium.From the data, the potassium requirement for maintenance of the heifers was estimated to be 133 meq potassium daily per 100 kg body weight.

1990 ◽  
Vol 258 (5) ◽  
pp. F1401-F1408 ◽  
Author(s):  
D. R. Martin ◽  
J. B. Pevahouse ◽  
D. J. Trigg ◽  
D. L. Vesely ◽  
J. E. Buerkert

The present investigation was designed to determine whether peptides derived from the NH(2)-terminal portion of the 126-amino acid prohormone (pro) of atrial natriuretic factor (ANF) have natriuretic and diuretic properties similar to ANF. Three peptides consisting of amino acids 1-30 [(proANF-(1-30)], 31-67 [proANF-(31-67)], and 79-98 (proANF-(79-98)] of the ANF prohormone were tested and compared with the COOH-terminus peptide (ANF) with respect to their ability to increase urine volume, urine sodium and potassium excretion, and glomerular filtration rate (GFR) in anesthetized Munich-Wistar rats. Each of these peptides except proANF-(79-98) caused a significant diuresis (P less than 0.05) when infused at their respective 100 ng.kg body wt-1.min-1 concentrations for 120 min. ProANFs-(1-30), (31-67), (79-98), and (99-126) (ANF) increased sodium excretion by 231, 973, 167, and 1,405%, respectively. The fractional excretion of sodium compared with control was significant at P less than 0.05, P less than 0.01, and P less than 0.05 for proANFs (1-30), (31-67), and (99-126), respectively. ProANF-(79-98) did not significantly increase the fractional excretion of sodium, but it was the only peptide from the NH(2)-terminus of the prohormone that significantly increased the fractional excretion of potassium's ProANF-(31-67) did not increase urinary potassium excretion. ProANF-(1-30), (79-98), and ANF significantly (P less than 0.05) increased urinary potassium excretion. None of these peptides significantly enhanced GFR. In conclusion, three peptides from the NH(2)-terminus of the ANF prohormone as well as ANF (the COOH-terminus) have either natriuretic, kaliuretic, and/or diuretic properties, but the respective ability of each of these peptides to produce these effects varies considerably.


1988 ◽  
Vol 66 (11) ◽  
pp. 1420-1424 ◽  
Author(s):  
J. F. Templeton ◽  
V. P. Sashi Kumar ◽  
D. Bose ◽  
D. D. Smyth ◽  
R. S. Kim ◽  
...  

The synthesis of the glucoside, 3β-[(β-D-glucopyranosyl)oxy]-14-hydroxy-14β-pregn-4-en-20-one, a 14β-hydroxyprogesterone glucoside (14β-OHP-glu), is described. This compound has an IC50 of 1 μM in a [3H]ouabain binding assay, and is about 10 times more potent than the aglycone. Like 14β-hydroxyprogesterone, the glucoside enhances contractility of isolated cardiac muscle. 14β-OHP-glu or ouabain, when infused at comparable doses into the renal artery of the anesthetized rat, markedly increases urine volume. Whereas ouabain significantly enhances urinary potassium excretion with little or no effect on sodium excretion, 14β-OHP-glu promotes a marked natriuresis with no significant effect on potassium excretion.


2007 ◽  
Vol 292 (1) ◽  
pp. R625-R636 ◽  
Author(s):  
Helle C. Thiesson ◽  
Boye L. Jensen ◽  
Claus Bistrup ◽  
Peter D. Ottosen ◽  
Alison D. McNeilly ◽  
...  

Downregulation of the renal glucocorticoid-metabolizing enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2) during liver cirrhosis may allow activation of the mineralocorticoid receptor (MR) by glucocorticoids and contribute to sodium retention. We tested this hypothesis in male Wistar rats with decompensated liver cirrhosis and ascites 7 wk after bile duct ligation (BDL). Renal 11β-HSD-2 mRNA, protein, and activity were significantly decreased in decompensated rats. The urinary Na+/K+ ratio was reduced by 40%. Renal epithelial sodium channel (ENaC) mRNA and immunostaining were only slightly affected. Complete metabolic studies, including fecal excretion, showed that the BDL rats had avid renal sodium retention. Treatment of the BDL rats with dexamethasone suppressed endogenous glucocorticoid production, normalized total sodium balance and renal sodium excretion, and reduced ascites formation to the same degree as direct inhibition of MR with K-canrenoate. Total potassium balance was negative in the BDL rats, whereas renal potassium excretion was unchanged. In the distal colon, expression of ENaC was increased in BDL rats. Fecal potassium excretion was increased in cirrhotic rats, and this was corrected by treatment with K-canrenoate but not dexamethasone. We conclude that development of sodium retention and decompensation in cirrhotic rats is associated with downregulation of renal 11β-HSD-2 activity and inappropriate activation of renal sodium reabsorption by endogenous glucocorticoids. In addition, the overall potassium loss in the BDL model is due to increased fecal potassium excretion, which is associated with upregulation of ENaC in distal colon.


2019 ◽  
Vol 30 (8) ◽  
pp. 1425-1438 ◽  
Author(s):  
Peng Wu ◽  
Zhong-Xiuzi Gao ◽  
Dan-Dan Zhang ◽  
Xiao-Tong Su ◽  
Wen-Hui Wang ◽  
...  

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.


1969 ◽  
Vol 73 (3) ◽  
pp. 445-452 ◽  
Author(s):  
R. Paquay ◽  
F. Lomba ◽  
A. Lousse ◽  
V. Bienfet

SummaryStatistical analyses were carried out on the data obtained under strictly controlled conditions in metabolism stalls with 41 different rations fed to 127 adult non-pregnant dry cows, and with 14 other different rations fed to 35 adult non-pregnant lactating cows that had calved 2–6 months earlier and whose daily milk production ranged from 11 to 20 kg.The authors have calculated and studied the correlations between faecal and urinary potassium losses, potassium excretion in the milk, digestible potassium and potassium balance, and the 75 other nutritive factors which were analysed for each of the 55 above mentioned experimental diets.The results show that three nutritional factors, potassium, dry-matter and nitrogen intakes, influence the fate of dietary potassium. The apparent digestibility of potassium is hyperbolically related to potassium content of the diet since the true digestibility of potassium is very high, unrelated to potassium intake and rather constant and since about 2·2 g of endogenous potassium are excreted in the faeces per kg of ingested dry matter.The quantities of digestible potassium strongly influence both the potassium urinary outputs and potassium balance. An increase in digestible dry matter enhances too the urinary potassium excretion as well as faecal output and lower potassium balance twice as much.But the most interesting feature in the potassium metabolism is that at any level, ingestion, digestion, excretion, there is a very close correlation between potassium and nitrogen.


1989 ◽  
Vol 76 (2) ◽  
pp. 213-219 ◽  
Author(s):  
Aaron Spital ◽  
Richard H. Sterns

1. Prior adaptation to a high potassium (HK) diet reduces the increment in plasma potassium after nephrectomy and acute potassium loading. Previous work has suggested that this ‘extrarenal potassium adaptation’ is due to direct stimulation of cellular potassium uptake by chronic hyperaldosteronism. 2. In contrast, we have shown that when dietary potassium is withdrawn from HK rats, large urinary potassium losses persist, resulting in ‘paradoxical potassium depletion’. This potassium depletion facilitates cellular potassium uptake and is, at least in part, responsible for extrarenal potassium adaptation. 3. To try to reconcile these observations, we explored further the role of aldosterone in extrarenal potassium adaptation. When dietary potassium was withdrawn from chronically adrenalectomized HK rats, paradoxical potassium depletion was markedly blunted and extrarenal potassium adaptation could not be demonstrated. Similarly, urinary potassium losses and potassium depletion were reduced when acute adrenalectomy was performed concomitantly with dietary potassium withdrawal. 4. We were unable to confirm previous studies showing extrarenal potassium adaptation in the absence of potassium depletion. Thus, extrarenal potassium adaptation did not occur after pretreatment with chronic high-dose mineralocorticoid, after prior adaptation to a sodium-free diet, or after prior adaptation to an extremely HK diet in the absence of dietary potassium withdrawal. 5. We conclude that chronic hyperaldosteronism is important in extrarenal potassium adaptation, but probably not via direct enhancement of cellular potassium uptake. Rather, in HK animals, hyperaldosteronism magnifies urinary potassium losses during fasting and thus promotes potassium depletion, which in turn facilitates the uptake of an acute potassium load.


1978 ◽  
Vol 235 (3) ◽  
pp. R175-R180 ◽  
Author(s):  
F. M. Sulzman ◽  
C. A. Fuller ◽  
L. G. Hiles ◽  
M. C. Moore-Ede

The relative contributions of light-dark (LD) cycles and feeding (EF) cycles in providing temporal information to the circadian time-keeping system were examined in chair-acclimatized squirrel monkeys (Saimiri sciureus). The circadian rhythms of drinking, colonic temperature, urine volume, and urinary potassium excretion were measured with the LD and EF cycles providing either conflicting phases or periods. In conflicting phase experiments, animals were exposed to 24-h LD cycles consisting of 12 h of 600 lx followed by 12 h of less than 1 ls and concurrent 24-h EF cycles in which the animals ate for 3 h and then fasted for 21 h. One group had food available at the beginning and a second group at the end of the light period. In conflicting period experiments, monkeys were exposed to 23-h LD cycles (LD 11.5:11.5) and 24-h EF cycles (EF 3:21). Analysis of the rhythms showed that both phase and period information were conveyed to the drinking and urinary rhythms by the EF cycle, and to the temperature rhythm by the LD cycle.


1985 ◽  
Vol 68 (5) ◽  
pp. 601-604 ◽  
Author(s):  
A. Barden ◽  
L. J. Beilin ◽  
R. Vandongen ◽  
I. Rouse

1. Measurement of urinary 6-ketoprostaglandin (PG) F1α and PGE2 excretion in 83 healthy children, aged 5-15 years, revealed that supervised 4 h urine collections under mild water diuresis provided more consistent results than overnight 12 h urine collections. 2. Males had higher urinary excretion of 6-keto-PGF1α but not of PGE2 compared with females. 3. Urinary potassium was related to 6-keto-PGF1α in both 4 and 12 h urine collections and urinary sodium to 6-keto-PGFα in 4 h collections only. 4. In the sexes combined multiple regression analyses revealed age as the only significant influence on prostanoid excretion (P = 0.001). 5. Thus age and sex and dietary potassium intake need to be considered in studies of urinary prostanoids in children.


1984 ◽  
Vol 246 (3) ◽  
pp. F300-F308 ◽  
Author(s):  
W. R. Adam ◽  
G. J. Goland ◽  
R. M. Wellard

This study examines the role of adrenocortical hormones in the kaliuresis following an acute intragastric KCl load in conscious control (CK) and high potassium diet (HK) rats. Adrenalectomy, 1 day before test, reduced K+ excretion by 35% in CK and 60% in HK rats, leading to minimal differences in K excretion between CK and HK. By contrast, spironolactone inhibited K excretion by only 10%. Glucocorticoids (dexamethasone 3-10 micrograms/100 g) increased K+ excretion in adrenalectomized CK and to a greater extent in adrenalectomized HK rats. Aldosterone (3 micrograms/100 g) alone had a variable effect on urinary potassium excretion in adrenalectomized rats. A combination of dexamethasone (3 micrograms/100 g) and aldosterone (3 micrograms/100 g) in adrenalectomized rats induced potassium excretion equivalent to that in intact rats. Adrenalectomized HK rats had a greater kaliuretic response to dexamethasone and aldosterone than CK rats. These results 1) demonstrate a role for glucocorticoids in K+ excretion in HK rats and 2) illustrate the importance of the increased responsiveness to both glucocorticoids and mineralocorticoids in potassium adaptation.


2020 ◽  
Vol 13 (6) ◽  
pp. 952-968
Author(s):  
Kuang-Yu Wei ◽  
Martin Gritter ◽  
Liffert Vogt ◽  
Martin H de Borst ◽  
Joris I Rotmans ◽  
...  

Abstract Potassium often has a negative connotation in Nephrology as patients with chronic kidney disease (CKD) are prone to develop hyperkalaemia. Approaches to the management of chronic hyperkalaemia include a low potassium diet or potassium binders. Yet, emerging data indicate that dietary potassium may be beneficial for patients with CKD. Epidemiological studies have shown that a higher urinary potassium excretion (as proxy for higher dietary potassium intake) is associated with lower blood pressure (BP) and lower cardiovascular risk, as well as better kidney outcomes. Considering that the composition of our current diet is characterized by a high sodium and low potassium content, increasing dietary potassium may be equally important as reducing sodium. Recent studies have revealed that dietary potassium modulates the activity of the thiazide-sensitive sodium-chloride cotransporter in the distal convoluted tubule (DCT). The DCT acts as a potassium sensor to control the delivery of sodium to the collecting duct, the potassium-secreting portion of the kidney. Physiologically, this allows immediate kaliuresis after a potassium load, and conservation of potassium during potassium deficiency. Clinically, it provides a novel explanation for the inverse relationship between dietary potassium and BP. Moreover, increasing dietary potassium intake can exert BP-independent effects on the kidney by relieving the deleterious effects of a low potassium diet (inflammation, oxidative stress and fibrosis). The aim of this comprehensive review is to link physiology with clinical medicine by proposing that the same mechanisms that allow us to excrete an acute potassium load also protect us from hypertension, cardiovascular disease and CKD.


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