Effect of plasma [K+] on the DC potential and on ion distributions between CSF and blood

1975 ◽  
Vol 39 (6) ◽  
pp. 1012-1016 ◽  
Author(s):  
S. W. Bledsoe ◽  
A. H. Mines
Keyword(s):  
Potassium Concentration ◽  
Electrical Potential ◽  
Fold Increase ◽  
Plasma Potassium ◽  
Electrical Potential Difference ◽  
Control Value ◽  
Ion Distributions ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Effective Role

Keeping the arterial pH at 7.4 and PaCO2 at 40 mmHg in eight anesthetized dogs, we acutely raised plasma potassium concentration from 3.4 to 8.2 meq/1, then allowed it to decay back to control levels. The cerebrospinal fluid (CSF)-blood electrical potential difference (pd) increased 13.2 mV per 10-fold increase in plasma [K+]. Again keeping arterial pH at 7.4 and PaCO2 at 40 mmHg, we elevated plasma [K+] in four dogs from 3.3 to 8.0 meq/1 and maintained this level for 6 h. We found 1) that the PD increased from a control value of +1.3 to +8.9mV, showing no tendency to decay over the 6 h; and 2) that the change in PD did not affect the distribution of Na+, K+, H+, Cl-, or HCO3- between blood and CSF over the 6 h. These results suggest that under these conditions the PD between CSF and blood may play no effective role in determining the distributions of these charged species by 6 h. These results are contrasted with recent findings which suggest that H+ and HCO3- are distributed according to passive forces between CSF and blood.

Regulation of extracellular potassium in hypothermia

1963 ◽  
Vol 205 (6) ◽  
pp. 1285-1289 ◽  
Author(s):  
G. S. Kanter
Keyword(s):  
Renal Function ◽  
Renal Tubule ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Extracellular Ph ◽  
Extracellular Potassium ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Intracellular Metabolism ◽  
K Concentration

Reduction of rectal temperature by ice packing in anesthetized dogs resulted in a fall in plasma potassium concentration in spite of the fall in arterial pH. Such a decrease in extracellular pH in normothermia would cause an increase in plasma K concentration. It was suggested that due to previously shown depression of renal acidification mechanisms in hypothermia, there occurred a K+ for Na+ exchange in the renal tubule with K+ being excreted instead of H+. It was expected that removal of renal function during hypothermia would allow the alteration in pH to cause an increase in extracellular K. Renal function was therefore removed by bilateral nephrectomy in five dogs and by ligation of both ureters in four dogs. Contrary to expectations, it was found that in the absence of renal function during hypothermia plasma K still fell markedly. No difference was found in the nephrectomized or ureter-tied dogs. It was proposed that in hypothermia, in the absence of renal function, some function of intracellular metabolism controlled extracellular K. Possibly intracellular pH decreased relatively more than did extracellular pH with a resultant movement of H+ out of the cell and K+ in. With renal function present in hypothermia, the influx of K into the cell seen in nephrectomized and ureter-tied dogs is reversed by the renal gradient which causes both a decrease in cellular and extracellular K.

Acid-base alterations and plasma potassium concentration

1959 ◽  
Vol 197 (2) ◽  
pp. 319-326 ◽  
Author(s):  
Daniel H. Simmons ◽  
Melvin Avedon
Keyword(s):  
Steady State ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Alveolar Ventilation ◽  
Acid Base ◽  
Blood Ph ◽  
Arterial Ph ◽  
Significant Difference ◽  
Anesthetized Dogs ◽  
K Concentration

Arterial pH of anesthetized dogs was held constant during infusion of HCl or NaHCO3 by appropriate alterations in alveolar ventilation. While plasma potassium concentration dropped somewhat (presumably due to gradual potassium depletion), there was no significant difference in plasma potassium during the two types of infusions. The implication is that metabolic and respiratory acid-base disturbances having comparable effects on pH also have similar effects on the plasma potassium concentration. Other data support this conclusion and also indicate that effects of acidosis and alkalosis are quantitatively similar. On the basis of data of this study and of other data in the literature, it appears that the ratio of change in potassium concentration to change in blood pH ordinarily averages –3.0 to –5.0 in a steady state and that achieving a steady state requires 1–2 hours of equilibration. Data are presented which support the concept that extracellular K concentration, rather than total extracellular K, is physiologically regulated and that this involves rapid exchanges with intracellular K.

Effects of changes in electrical potential difference on tubular potassium transport

1980 ◽  
Vol 238 (3) ◽  
pp. F235-F246 ◽  
Author(s):  
E. Garcia-Filho ◽  
G. Malnic ◽  
G. Giebisch
Keyword(s):  
Potassium Concentration ◽  
Electrical Potential ◽  
Potential Drop ◽  
Plasma Potassium ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
High Potassium ◽  
Transepithelial Potential ◽  
Wide Range ◽  
Potassium Secretion

To assess directly the role of the transepithelial potential difference (PD) on potassium concentration differences across distal tubular epithelium, continuous and stationary microperfusion experiments were done in tubules voltage-clamped over a wide range of lumen-negative potentials. Potassium was measured either chemically or in situ by potassium-sensitive microelectrodes. Distal cell PD measurements show that most of the potential drop induced by luminal current injection occurred across the luminal cell membrane. Experiments were done in rats either on a control or on a high potassium diet and after amiloride administration. Luminal potassium was highly sensitive to imposed electrical potential changes, attainment of a new steady-state intraluminal potassium concentration was rapid (less than 1 s), and higher luminal potassium concentrations were observed in animals in which potassium secretion had been stimulated. Similar slopes of tubular fluid-to-plasma potassium ratios versus transepithelial potential differences were observed in all experiments. All slopes intersected, at zero PD, at a luminal tubular fluid-to-plasma concentration ratio in excess of unity, indicating the presence of an active component of potassium secretion.

Relationship of hepatic potassium efflux to phosphorylase activation induced by glucagon

1964 ◽  
Vol 206 (4) ◽  
pp. 738-742 ◽  
Author(s):  
Anthony G. Finder ◽  
Theodore Boyme ◽  
William C. Shoemaker
Keyword(s):  
Time Course ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Potassium Efflux ◽  
Blood Samples ◽  
Potassium Release ◽  
Anesthetized Dogs ◽  
Relationship Of ◽  
Primary Action ◽  
Made In

Hepatic biopsies were obtained from intact, anesthetized dogs before and at 6- to 15-sec intervals after intravenous administration of glucagon. Simultaneously, blood samples were taken from the hepatic vein at 3-sec intervals and the plasma potassium concentration measured. The time course of phosphorylase activation in hepatic biopsies was observed and compared with the time course of potassium release into the hepatic efflux. Measurements were made in normothermic (38 C) animals and in animals subjected to hypothermia (21–25 C). Maximum phosphorylase activation was reached in an average of 79 sec in normothermia and in 144 sec in hypothermia. Maximum hepatic venous potassium concentrations were observed in an average of 41 sec in normothermia and 108 sec in hypothermia. The increased hepatic potassium release which preceded the activation of phosphorylase suggested that electrolyte shifts may be involved in the primary action of glucagon upon hepatic glycogenolytic systems.

Respiratory alkalosis and hypokalemia in dogs exposed to simulated high altitude

1962 ◽  
Vol 202 (6) ◽  
pp. 1041-1044 ◽  
Author(s):  
D. C. Smith ◽  
J. Q. Barry ◽  
A. J. Gold
Keyword(s):  
High Altitude ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Respiratory Alkalosis ◽  
Simulated Altitude ◽  
Simulated High Altitude ◽  
Anesthetized Dogs ◽  
Per Se ◽  
Decompression Stress

Exposure of restrained, unanesthetized dogs to a simulated altitude of 30,000 ft consistently resulted in respiratory alkalosis and marked hypokalemia. When alkalosis was prevented by increasing the pCO2 of inspired air during decompression, a smaller but statistically significant decrease in plasma potassium concentration still occurred. In comparison with previous studies, the hypokalemia observed in these restrained, unanesthetized dogs was greater than that found in either unrestrained or anesthetized dogs subjected to the same decompression stress. Consequently, the suggestion is made that in the unanesthetized, restrained dog, the hypokalemic response not attributable to respiratory alkalosis is of adrenal mediation and results from the "stress" of restraint plus hyperventilation, rather than to hypoxemia or the decompression stress, per se.

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.

Stimulation of renin secretion by vasoactive intestinal peptide

1982 ◽  
Vol 243 (3) ◽  
pp. F306-F310
Author(s):  
J. P. Porter ◽  
I. A. Reid ◽  
S. I. Said ◽  
W. F. Ganong
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Vasoactive Intestinal Peptide ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Renin Secretion ◽  
Threefold Increase ◽  
Anesthetized Dogs ◽  
Stimulation Of

Vasoactive intestinal peptide (VIP) increased plasma renin activity (PRA) in pentobarbital-anesthetized dogs. A 15-min infusion of VIP directly into the renal artery at a dose of 33 ng . kg-1 min-1 increased renin secretion rate from 1,461 +/- 393 to 5,769 +/- 1,794 ng ANG I . ml-1 . 3 h-1 . min-1, and increased PRA from 19.2 +/- 2.3 to 29.2 +/- 4.7 ng ANG I . ml-1 . 3 h-1. Renal blood flow and creatinine clearance were also increased, whereas plasma potassium concentration and diastolic blood pressure decreased. There was no change in sodium or potassium excretion. When administered intravenously, 33 and 13 ng . kg-1 . min-1 VIP increased PRA. A dose of 3.3 ng . kg-1 . min-1 failed to increased PRA when given intravenously but produced a significant increase in PRA from 22.8 +/- 8.1 to 40.5 +/- 19.4 ng ANG I . ml-1 . 3 h-1 when infused into the renal artery. This increase occurred without any change in plasma potassium concentration or blood pressure. Renin secretion was increased by a two- to threefold increase in plasma VIP; comparable increases in plasma VIP have been reported to be produced by various experimental procedures. The data indicate that VIP increases renin secretion. The peptide appears to act directly on the kidney and may act directly on the juxtaglomerular cells.

scholarly journals The K+-driven Amino Acid Cotransporter of the Larval Midgut of Lepidoptera: Is Na+ an Alternative Substrate

1992 ◽  
Vol 162 (1) ◽  
pp. 281-294
Author(s):  
G. M. HANOZET ◽  
V. F. SACCHI ◽  
S. NEDERGAARD ◽  
P. BONFANTI ◽  
S. MAGAGNIN ◽  
...  
Keyword(s):  
Amino Acid ◽  
Electrical Potential ◽  
Membrane Vesicles ◽  
Electrical Potential Difference ◽  
Glycine Uptake ◽  
Larval Midgut ◽  
Control Value ◽  
Fixed Concentration ◽  
K Concentration ◽  
Transmembrane Electrical Potential

Amino acid accumulation within brush-border membrane vesicles (BBMV) from the larval midgut of Lepidoptera is driven by a K+ gradient. However, it can also be driven by a Na+ gradient, although with reduced efficiency. To examine the possibility that sodium and potassium ions are handled by the same amino acid transporter, glycine uptake into BBMV from Philosamia cynthia Drury was measured in the presence of a pH gradient and of a transmembrane electrical potential difference, i.e. in simulated ‘physiological’ conditions. The kinetics of glycine uptake at extravesicular saturating Na+ or K+ concentrations discloses a higher affinity of the cotransporter for the amino acid in the presence of Na+ but a maximum transport rate with K+. Glycine uptake at a fixed concentration as a function of external Na+ or K+ concentration yields curves that show saturation but do not fit a rectangular hyperbola, with Hill coefficients less than 1 with Na+ and greater than 1 with K+. These coefficients vary according to glycine concentration. Increasing the concentration of extravesicular Na+ at a saturating external K+ concentration reduced glycine uptake to 70% of the control value. This inhibition curve is compatible with competition between the two cations for the same cotransporter and with the presence of different kinetic constants with Na+ or K+. The data are consistent with a steady-state random two-substrate mechanism for glycine transport, with Na+ and K+ as alternative substrates.

Transepithelial voltage changes during prostatic secretion in the dog

1983 ◽  
Vol 245 (4) ◽  
pp. F470-F477
Author(s):  
E. R. Smith ◽  
T. B. Miller ◽  
R. F. Pebler
Keyword(s):  
Venous Blood ◽  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Transcellular Transport ◽  
Prostatic Fluid ◽  
Maximum Change ◽  
Anesthetized Dogs ◽  
Transepithelial Voltage ◽  
Time Courses

To define the nature of Na+, K+, and Cl- secretion by the dog prostate, the electrical potential difference between fluid in the prostatic urethra and venous blood was recorded during secretion provoked in pentobarbital-anesthetized dogs by electrically stimulating the hypogastric nerves or by administering pilocarpine intravenously. The resultant prostatic fluid samples as well as plasma samples taken before and/or after secretion were analyzed for these electrolytes. During secretion provoked by either means the transepithelial electrical potential difference, which was essentially zero at rest, became lumen negative, the maximum change (which was related to gland size) being about 4 mV. The time courses of both the potential change and the secretion of fluid were very similar. The Na+ concentration in both nerve- and pilocarpine-induced prostatic fluid was equal to that in plasma, whereas the K+ and Cl- concentrations were higher than in plasma. It is concluded that Na+ may move passively from plasma into prostatic fluid, perhaps via the paracellular route, but the movement of K+ and Cl- probably involves active transcellular transport.

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