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J B Russell - One of the best experts on this subject based on the ideXlab platform.

  • the ability of low g c gram positive ruminal bacteria to resist monensin and counteract Potassium Depletion
    Current Microbiology, 1999
    Co-Authors: Todd R Callaway, Kristin A Adams, J B Russell
    Abstract:

    Gram-negative ruminal bacteria with an outer membrane are generally more resistant to the feed additive, monensin, than Gram-positive species, but some bacteria can adapt and increase their resistance. 16S rRNA sequencing indicates that a variety of ruminal bacteria are found in the "low G + C Gram-positive group," but some of these bacteria are monensin resistant and were previously described as Gram-negative species (e.g., Selenomonas ruminantium and Megasphaera elsdenii). The activity of monensin can be assayed by its ability to cause Potassium loss, and results indicated that the amount of monensin needed to catalyze half maximal Potassium Depletion (K(d)) from low G + C gram-positive ruminal bacteria varied by as much as 130-fold. The K(d) values for Butyrivibrio fibrisolvens 49, Streptococcus bovis JB1, Clostridium aminophilum F, S. ruminantium HD4, and M. elsdenii B159 were 10, 65, 100, 1020, and 1330 nM monensin, respectively. B. fibrisolvens was very sensitive to monensin, and it did not adapt. S. bovis and C. aminophilum cultures that were transferred repeatedly with sub-lethal doses of monensin had higher K(d) values than unadapted cultures, but the K(d) was always less than 800 nM. S. ruminantium and M. elsdenii cells were highly resistant (K(d) > 1000 nM), and this resistance could be explained by the ability of these low G + C Gram-positive bacteria to synthesize outer membranes.

  • use of Potassium Depletion to assess adaptation of ruminal bacteria to ionophores
    Applied and Environmental Microbiology, 1996
    Co-Authors: R P Lana, J B Russell
    Abstract:

    When mixed ruminal bacteria from cattle fed timothy hay were suspended in a medium containing a low concentration of Potassium, monensin and lasalocid catalyzed a rapid Depletion of Potassium from cells. The ionophore-mediated Potassium Depletion was concentration dependent, and it was possible to describe the relationship with saturation constants. Mixed ruminal bacteria never lost more than 50% of their Potassium (Kmax = 46%), and the concentrations of monensin and lasalocid needed to cause half-maximal Potassium Depletion (Kd) were 178 and 141 nM, respectively. When cattle were fed 350 mg of monensin per day, the ratio of ruminal acetate to propionate decreased from 4.2 to 2.9, and the Kd of monensin was eightfold greater than the value for mixed ruminal bacteria from control animals. Monensin supplementation also caused a twofold increase in the Kd of lasalocid. Lasalocid supplementation (350 mg per day) had no effect on the ruminal acetate-to-propionate ratio, but it caused a twofold increase in the Kd values of monensin and lasalocid. Increases in Kd occurred almost immediately after ionophore was added to the ration, and the Kd values returned to their prefeeding values within 14 days of withdrawal. Ionophore supplementation had no effect on the Kmax values, and approximately 50% of the population was always highly ionophore resistant. Because the Kd values of even adapted ruminal bacteria were low (< 1.5 microM), it appears that a large proportion of the ruminal ionophore is bound nonselectively to feed particles or ionophore-resistant bacteria.

Prida Malasit - One of the best experts on this subject based on the ideXlab platform.

  • proteomic identification of altered proteins in skeletal muscle during chronic Potassium Depletion implications for hypokalemic myopathy
    Journal of Proteome Research, 2006
    Co-Authors: Visith Thongboonkerd, Rattiyaporn Kanlaya, Supachok Sinchaikul, Paisal Parichatikanond, Shuitein Chen, Prida Malasit
    Abstract:

    Prolonged Potassium Depletion is a well-known cause of myopathy. The pathophysiology of hypokalemic myopathy, however, remains unclear. We performed a gel-based, differential proteomics study to define altered proteins in skeletal muscles during chronic Potassium Depletion. BALB/c mice were fed with normal chow (0.36% K+) or K+-depleted (KD) diet (<0.001% K+) for 8 weeks (n = 5 in each group). Left gastrocnemius muscles were surgically removed from each animal. Histopathological examination showed mild-degree infiltration of polymornuclear and mononuclear cells at the interstitium of the KD muscles. Extracted proteins were resolved with two-dimensional electrophoresis (2-DE), and visualized with Coomassie Brilliant Blue R-250 stain. Quantitative intensity analysis revealed 16 up-regulated protein spots in the KD muscles, as compared to the controls. These differentially expressed proteins were subsequently identified by peptide mass fingerprinting and by quadrupole time-of-flight tandem mass spectrometry ...

Patricio E. Ray - One of the best experts on this subject based on the ideXlab platform.

  • chronic Potassium Depletion induces renal injury salt sensitivity and hypertension in young rats
    Kidney International, 2001
    Co-Authors: Patricio E. Ray, Shinichi Suga, Xuehui Liu, Xiuling Huang, Richard J Johnson
    Abstract:

    Chronic Potassium Depletion induces renal injury, salt sensitivity, and hypertension in young rats. Background Chronic hypokalemia has been associated with renal hypertrophy, interstitial disease, and hypertension in both adult animals and humans. However, the effects of Potassium (K + ) Depletion on the rapidly growing infant have not been well studied. The purpose of this study was to determine the effects of severe chronic dietary K + Depletion on blood pressure (BP) and renal structural changes in young rats. Methods Sprague-Dawley rats (50 ± 5g) were fed either a control or a Potassium-deficient diet ( + ) for 14 to 21 days. At the end of this period, the blood pressure (BP) was measured in all rats, and six rats in each group were sacrificed to determine changes in renal histology and renin-angiotensin system (RAS) activity. The remaining rats in each group were then switched to a high-salt (6% NaCl)-normal-K + (0.5%) diet or were continued on their respective control or K + -deficient diet for an additional six days. Blood pressure measurements were done every three days until the end of the study. Results K + -depleted animals had significant growth retardation and increased RAS activity, manifested by high plasma renin activity, recruitment of renin-producing cells along the afferent arterioles, and down-regulation of angiotensin II receptors in renal glomeruli and ascending vasa rectae. K + -depleted kidneys also showed tubulointerstitial injury with tubular cell proliferation, osteopontin expression, macrophage infiltration, and early fibrosis. At week 2, K + -depleted rats had higher systolic BP than control rats. Switching to a high-salt (6% NaCl)-normal-K + diet resulted in further elevation of systolic BP in K + -depleted rats, which persisted even after the serum K + was normalized. Conclusion Dietary Potassium deficiency per se increases the BP in young rats and induces salt sensitivity that may involve at least two different pathogenic pathways: increased RAS activity and induction of tubulointerstitial injury.

  • Renal vascular induction of TGF-β2 and renin by Potassium Depletion
    Kidney international, 1993
    Co-Authors: Patricio E. Ray, Bryan K. Mccune, R. Ariel Gomez, Satoshi Horikoshi, Jeffrey B. Kopp, Paul E. Klotman
    Abstract:

    Renal vascular induction of TGF-β2 and renin by Potassium Depletion. Recently, we have found that transforming growth factor (TGF)-β2 and renin are abundantly expressed in the juxtaglomerular apparatus (JGA) of dehydrated mice. Since Potassium (K + ) Depletion also stimulates renin and induces hypertrophy of the JGA, we examined the ability of this maneuver to stimulate TGF-β isoforms and renin in renovascular tissue and the JGA of young rats. Sprague-Dawley rats (50 ± 5 g) were fed either a control diet or a Potassium-deficient diet ( + ) for 7, 16, or 21 days. As a control for TGF-β and renin stimulation, an additional group of animals was fed a normal diet but was water deprived for three days. Potassium-depleted animals experienced severe growth retardation but kidney weight increased significantly. Potassium Depletion induced both TGF-β2 and renin immunoreactivity in renal arterioles and the JGA but had no effect on TGF-β1 and TGF-β3 isoforms. To determine the role of circulating angiotensin II in the stimulation of TGF-β2 by Potassium Depletion, a group of Potassium-depleted rats received enalapril (100 mg/liter) in the drinking water. The addition of converting enzyme inhibitor increased both the intensity of TGF-β2 and renin staining as well as the number of cells positively stained. Our results demonstrate that K + Depletion induces TGF-β2 and renin in renal arterioles and in the JGA. Furthermore, circulating angiotensin II is not responsible for the increase in the local expression of TGF-β2. These findings suggest that TGF-β2 may be an important mediator of JGA hypertrophy. The simultaneous induction of TGF-β2 with renin suggests that these factors may be coregulated.

Robert J. Unwin - One of the best experts on this subject based on the ideXlab platform.

  • the relationship between distal tubular proton secretion and dietary Potassium Depletion evidence for up regulation of h atpase
    Nephrology Dialysis Transplantation, 1999
    Co-Authors: Matthew A. Bailey, Giovambattista Capasso, Samuel Agulian, G Giebisch, Robert J. Unwin
    Abstract:

    Background. Dietary Potassium Depletion is associated with elevated plasma bicarbonate concentration and enhanced bicarbonate reabsorption in the distal tubule. The relationship between distal proton secretion and Introduction Potassium status was investigated by in vivo microperfusion of the superficial distal tubule. The late distal tubule, consisting of the short conMethods. Experiments were performed on anaesthet- necting tubule and the initial portion of the cortical ized rats that had been maintained on either a low- collecting duct (CCD), typically displays a large, Potassium or control diet for 3‐5 weeks prior to lumen-negative transepithelial potential diVerence experimentation. The distal tubules were perfused at (V te ), of the order of 30‐50 mV. This lumen negativity 10 nl/min with either a standard or a barium chloride- arises primarily from the diVusion of Na+ into the containing solution, and the late distal tubular transepi- principal cell down a favourable electrochemical gradithelial potential diVerence ( V te ) and pH of the luminal ent (created by basolateral Na+,K+-ATPase activity), fluid were recorded using a double-barrelled voltage which depolarizes the apical membrane with respect to and ion-sensitive microelectrode. the basolateral membrane. Early studies found that Results. In control rats, the V te was ’40.7±2.4 mV when either Na+ or K+ transport was reduced (during and the tubular fluid pH was 6.44±0.07; in Potassium- luminal perfusion with amiloride, basolateral superfudepleted animals, the V te was ’15.0±1.4 mV and the sion with ouabain or in Na+- and K+-free solutions), pH was 6.76±0.03. The pH values in both groups the isolated rabbit CCD developed a stable, lumenof animals were significantly lower than would be positive V te [1,2]. The origin of the lumen-positive V te predicted from the V te and systemic pH for passive could not, therefore, be readily explained on the basis H+ distribution, indicating active proton secretion. of Na+ or K+ flux. However, if either acetazolamide Moreover, in hypokalaemic rats, this diVerence from or 4-acetamido-4ae-isothiocyanostilbene-2,2ae-disulfonic predicted pH was significantly greater than in con- acid (SITS) was added to the bath during simultaneous trol animals (control=0.27±0.06 vs low-Potassium= luminal perfusion with amiloride, the lumen positiv0.46±0.03; P<0.01), suggesting enhanced active ity was markedly attenuated [1,2]. Moreover, in the proton secretion. During perfusion with a solution absence of amiloride, these agents increased the lumencontaining BaCl 2 , the late distal tubule V te became negative potential diVerence. These experiments suglumen positive in Potassium-depleted rats, contrasting gested that acidification of the tubular fluid was, to a with an increased lumen negativity in Potassium-replete degree, electrogenic, providing a positive component controls. The barium-induced lumen-positive potential to the V te that is normally obscured by the larger, diVerence observed in the hypokalaemic rats was abol- negative potential resulting from the balance of Na+ ished by intravenous administration of acetazolamide. and K+ fluxes ( Figure 1). Conclusion. These data are consistent with enhanced In the present series of experiments, we have investielectrogenic proton secretion (H+-ATPase) during gated the contribution of electrogenic proton secretion dietary Potassium deprivation. to the development of late distal tubular V te in vivo. In addition, we have investigated the relationship between dietary Potassium Depletion, a condition asso

  • Upregulation of H+-ATPase in the distal nephron during Potassium Depletion: structural and functional evidence
    American Journal of Physiology-Renal Physiology, 1998
    Co-Authors: Matthew A. Bailey, Robert M. Fletcher, David F. Woodrow, Robert J. Unwin, Stephen J. Walter
    Abstract:

    In the present study, we have investigated the effects of dietary Potassium Depletion on the activity and distribution of the H+-ATPase in the distal nephron of the Sprague-Dawley rat. H+-ATPase activity was assessed from the change in transepithelial potential difference ( V te) in response to bafilomycin A1 during perfusion of the late distal tubule in vivo, with solutions containing inhibitors of known ion channels. Bafilomycin A1 caused a negative deflection in V te in control animals, an effect that was significantly enhanced during Potassium Depletion ( P < 0.01). The distribution of H+-ATPase within the population of intercalated cells was assessed using a specific monoclonal antibody (E11). Hypokalemia was associated with a highly significant redistribution of the staining pattern ( P < 0.001), with an increase in the percentage of cells displaying immunoreactivity in the apical membrane. These results indicate that dietary Potassium Depletion increases electrogenic H+-ATPase activity in the rat distal tubule; this may be associated with increased insertion of pumps into the apical membrane.

R P Lana - One of the best experts on this subject based on the ideXlab platform.

  • use of Potassium Depletion to assess adaptation of ruminal bacteria to ionophores
    Applied and Environmental Microbiology, 1996
    Co-Authors: R P Lana, J B Russell
    Abstract:

    When mixed ruminal bacteria from cattle fed timothy hay were suspended in a medium containing a low concentration of Potassium, monensin and lasalocid catalyzed a rapid Depletion of Potassium from cells. The ionophore-mediated Potassium Depletion was concentration dependent, and it was possible to describe the relationship with saturation constants. Mixed ruminal bacteria never lost more than 50% of their Potassium (Kmax = 46%), and the concentrations of monensin and lasalocid needed to cause half-maximal Potassium Depletion (Kd) were 178 and 141 nM, respectively. When cattle were fed 350 mg of monensin per day, the ratio of ruminal acetate to propionate decreased from 4.2 to 2.9, and the Kd of monensin was eightfold greater than the value for mixed ruminal bacteria from control animals. Monensin supplementation also caused a twofold increase in the Kd of lasalocid. Lasalocid supplementation (350 mg per day) had no effect on the ruminal acetate-to-propionate ratio, but it caused a twofold increase in the Kd values of monensin and lasalocid. Increases in Kd occurred almost immediately after ionophore was added to the ration, and the Kd values returned to their prefeeding values within 14 days of withdrawal. Ionophore supplementation had no effect on the Kmax values, and approximately 50% of the population was always highly ionophore resistant. Because the Kd values of even adapted ruminal bacteria were low (< 1.5 microM), it appears that a large proportion of the ruminal ionophore is bound nonselectively to feed particles or ionophore-resistant bacteria.