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

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.

1982 ◽  
Vol 242 (6) ◽  
pp. F599-F603 ◽  
Author(s):  
D. B. Young

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.


1984 ◽  
Vol 246 (6) ◽  
pp. F772-F778 ◽  
Author(s):  
D. B. Young ◽  
T. E. Jackson ◽  
U. Tipayamontri ◽  
R. C. Scott

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.


2022 ◽  
pp. 109980042110654
Author(s):  
María Correa-Rodríguez ◽  
Sara DelOlmo-Romero ◽  
Gabriela Pocovi-Gerardino ◽  
José-Luis Callejas-Rubio ◽  
Raquel Ríos-Fernández ◽  
...  

Purpose: The aim of this study was to investigate the association between dietary sodium, potassium, and sodium:potassium ratio and clinical disease activity parameters, damage accrual, and cardiovascular disease risk factors in a population of patients with systemic lupus erythematous (SLE). Research design and study sample: A cross-sectional study including a total of 280 patients was conducted (90.4% females; mean age 46.9 ± 12.85 years). Data collection: The SLE Disease Activity Index (SLEDAI-2K) and the SDI Damage Index were used to assess disease activity and disease-related damage, respectively. A 24-hour diet recall was used to estimate dietary intake of sodium and potassium. Results: Dietary sodium intake was significantly associated with anti-dsDNA ( β  =  −.005; 95% CI [.002 .008]; p = .001) and complement C4 level ( β  =  −.002; 95% CI [−.003, .000]; p = .039). Dietary potassium intake was also significantly associated with complement C3 level ( β  =  −.004; 95% CI [−.007, −.001]; p = .021). Multiple logistic regression models revealed a positive association between dietary sodium intake and the risk of having hsCRP > 3 ( p = .005) and an inverse association between dietary potassium intake and the risk of having hsCRP > 3 ( p = .004). Conclusions: SLE patients with higher dietary sodium and lower dietary potassium intakes had an increased risk of higher hsCRP. Dietary sodium intake was significantly associated with anti-dsDNA and complement C4 level, while dietary potassium intake was associated with complement C3 level, supporting that dietary sodium and potassium intakes might play a key role in markers related to disease activity in SLE patients.


1987 ◽  
Vol 253 (6) ◽  
pp. F1182-F1196 ◽  
Author(s):  
J. C. Rutledge ◽  
L. Rabinowitz

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.


1984 ◽  
Vol 105 (2) ◽  
pp. 239-244 ◽  
Author(s):  
Matsuhiko Hayashi ◽  
Shigetoshi Senba ◽  
Ikuo Saito ◽  
Waichi Kitajima ◽  
Takao Saruta

Abstract. To examine potassium homeostasis in diabetes mellitus, we observed the effect of dietary potassium loading on the renin-angiotensin-aldosterone system and potassium balance in streptozotocin-induced diabetic rats. In diabetic rats with 26.51 ± 1.89 mmol/l of serum glucose, the plasma renin activity (PRA), plasma aldosterone (PA), immunoreactive insulin (IRI) and urinary excretion of prostaglandin E2 (PGE2) were all significantly lower than in control rats, but the plasma potassium and renal function were not significantly different. With potassium loading, both control and diabetic rats showed a similar increase in plasma potassium and urinary potassium excretion and a decrease in PRA, but the IRI, plasma corticosterone and urinary excretion of PGE2 exhibited no significant change. On the other hand, the PA was significantly increased only in the control rats, and not in the diabetic rats on potassium loading. Based up on these results, it is suggested that potassium homeostasis is well maintained in diabetic rats with normal renal function in spite of an attenuated response of aldosterone secretion to dietary potassium loading and insulin deficiency.


2007 ◽  
Vol 267 ◽  
pp. 1-3

In a nutshellDietary potassium intake is protective against heart disease in observational studies, particularly for hypertension and stroke.A number of RCTs (but not all) have shown that extra dietary potassium can lower BP, particularly when combined with adequate magnesium and a lowering of sodium intake.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Xiao Gu ◽  
Lesley F Tinker ◽  
Alison E Field ◽  
Mary B Roberts ◽  
Matthew Allison ◽  
...  

Background: Previous studies have suggested that sodium reduction could be a viable strategy for reducing heart failure-related disease burden. Relatively few studies had been conducted on dietary sodium and the incidence of heart failure (HF) and its major subtypes; HF with preserved ejection function (HFpEF) and HF with reduced ejection function (HFrEF). Hypothesis: We hypothesized that dietary sodium was positively associated with the risk of HF and its major subtypes with a linear dose-response relationship, whereas dietary potassium was inversely associated with the risks of these outcomes. Methods: Our observational cohort study included 118,057 racial/ethnically diverse postmenopausal women recruited during 1993-1998 and followed up until 2015 in the Women’s Health Initiative. Women who reported a history of HF, were underweight, or had implausible/missing food frequency questionnaire (FFQ) data were excluded at baseline. The exposures of our study were FFQ-measured dietary sodium and potassium calibrated by recovery biomarkers estimated from 24-hour urine excretion collections. The main outcomes were hospitalized heart failure, including HFpEF and HFrEF subtyping, as adjudicated by trained physicians. Results: During up to 22 years of follow-up, 2,533, 1,048 and 673 participants developed HF, HFpEF and HFrEF, respectively. The mean age of the study population was 63.4 years, in which 84.3% (99,297 of 118,057) were white, 7.8% (9,150 of 118,057) were African American, 3.8% (4,469 of 118,057) were Hispanic and 4.1% (4,832 of 118,057) were other race/ethnicity groups. The median of calibrated dietary sodium intake was 2,712.4 mg/day (interquartile range: 2,503.3 mg/day-2,948.4 mg/day) and the median of dietary potassium intake was 2,494.5 mg/day (interquartile range: 2,249.8 mg/day-2,718.2 mg/day). After adjusting for potential confounding variables and risk factors of HF, calibrated sodium intake was positively associated with the incidence of HF (HR Q5 vs. Q1 =2.59, 95% CI: 2.26-2.98, P-trend <0.001). Comparing extreme quintiles of sodium intake, the HR was 2.87 for HFpEF (95% CI: 2.29-3.60) and 1.71 for HFrEF (95% CI: 1.28-2.30, both P-trend<0.001). The dose-response relationships between calibrated sodium intake and the risk of HF and HFrEF were non-linear with accelerated increasing risks at higher intake level, while the dose-response relationship for HFpEF was linear. Similar positive associations were observed for the analyses on calibrated sodium/potassium ratio, whereas calibrated potassium intake was not associated with the risk of HF and its major subtypes. Conclusions: Higher sodium intake is associated with increased risk of HF and its major subtypes. The observed positive association appears to be stronger for HFpEF than for HFrEF. These findings help to inform dietary recommendations for primary heart failure prevention.


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.


1981 ◽  
Vol 61 (s7) ◽  
pp. 77s-80s ◽  
Author(s):  
Osamu Iimura ◽  
Toshiaki Kijima ◽  
Kenjiro Kikuchi ◽  
Akiyoshi Miyama ◽  
Toshiaki Ando ◽  
...  

1. In order to confirm and investigate the hypotensive effect of a high potassium intake we compared mean arterial pressure (MAP), water and electrolyte balance, plasma and urinary noradrenaline (NA), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in 20 inpatients with mild or moderate essential hypertension on a control diet (Na: 260, K: 75 mmol/day), and after high (K: 175 mmol/day) and low potassium diets (K: 25 mmol/day). 2. After potassium loading, urinary volume (UV) and urinary excretion of sodium (UNaV) and of potassium (UKV) were elevated, and MAP, body weight, plasma volume (PV), extracellular fluid volume (ECFV) and total exchangeable sodium (Nae) were reduced significantly. 3. After potassium loading, PRA, PAC, plasma and urinary NA increased and the pressor response to infused noradrenaline and angiotensin II decreased significantly. 4. The reduction of MAP after potassium loading correlated positively with PV and ECFV during the control period. In addition, significant correlations were found between ΔUV and ΔUNaV, —ΔPV and ΔU/NaV, —ΔPV and Δ plasma NA, and Δ plasma NA and Δ PRA. 5. Patients with low PRA had high PV, ECFV and Nae during the control period, and showed greater reductions of MAP, PV, ECFV and Nae after potassium loading. 6. After potassium restriction, UNaV, PRA and urinary NA decreased and PV increased, and MAP did not change significantly. 7. These results suggest that the hypotensive effect of high potassium intake may be caused by reduction of body fluid volume via augmentation of Na excretion.


2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Verena Hasenegger ◽  
Petra Rust ◽  
Kristina Englert ◽  
Jürgen König

AbstractIntroductionBeing the predominant osmotically active element inside cells, potassium is a central regulator of the osmotic balance and the electrochemical membrane potential. As such, it has an effect on blood pressure and therefore counteracts the effects of excess dietary sodium intake. Furthermore, potassium affects glucose homeostasis by influencing insulin secretion from the pancreatic β-cells. Due to the health-promoting effects of potassium, the German-speaking countries have recently updated the reference values for potassium. The revised estimates of adequate potassium intake are 4000 mg/d instead of previously recommended 2000 mg/d. However, a typical Western diet on average contains less potassium and more sodium.Materials and methodsThe presented data were collected within the Austrian Study on Nutrition 2014/2016, a regularly conducted representative cross-sectional survey to monitor food consumption in Austria. Altogether, data from 2129 adults aged between 18 and 64 years were included in the analysis. In the course of two years, and thus with the consideration of seasonal variations, the survey was conducted on the basis of two non-consecutive 24 hour recalls in accordance with the guidelines of the European Food Safety Authority (EFSA). The survey was approved by the Ethical Committee of the University of Vienna (reference number: 00284).ResultsAfter exclusion of misreporters the final sample consisted of 2018 individuals, of which 1282 (63.5%) were women. The mean age was 38.8 ± 11.9 years.Median dietary potassium intake was 2783 mg/d (IQR: 1245). Men had a higher median intake than women (3018 mg/d (IQR: 1303) vs. 2546 mg/d (IQR: 1112), p < 0.001). Significant differences between sexes existed in all age groups (p < 0.001). However, there was no significant correlation between age and dietary potassium intake.The estimates of adequate potassium intake of 4000 mg/d (DGE et al., 2017) were met by only 13.3% of the participants, 7.4% of women and 19.2% of men. Moreover, only 479 participants (23.8%, 16.7% of women and 30.9% of men) had intakes equal to or above 3500 mg/d, the adequate intake established by EFSA (2016).DiscussionOur data show that potassium intake has to be improved in all gender and age groups by increasing the consumption of potassium-rich foods. However, since the estimates of adequate potassium intake have doubled recently, it seems even more difficult to achieve these recommendations in daily food routine.


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