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.

Potassium loss from the heart during the immediate posthypercapnic period

1960 ◽  
Vol 198 (5) ◽  
pp. 962-964 ◽  
Author(s):  
E. B. Brown ◽  
Albert Mowlem
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Coronary Sinus ◽  
Coronary Flow ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Blood Oxygen ◽  
Blood Samples ◽  
Significant Difference ◽  
Coronary Sinus Blood

Experiments have been carried out on mongrel dogs in which plasma potassium concentrations in blood samples simultaneously drawn from the aorta and coronary sinus have been determined before, during and following 4 hours of high CO2 breathing. No significant difference between potassium concentration in aorta and coronary sinus blood was evident before or during breathing of high CO2 mixtures. Five minutes after returning to air breathing however, coronary sinus plasma potassium concentration was significantly elevated above that of the aorta. This loss of potassium from the heart is accompanied by severe cardiac irregularities, premature systoles, ventricular tachycardia and, sometimes, ventricular fibrillation. Coronary blood oxygen concentration differences decrease significantly during hypercapnia, and estimates by the N2O technique indicate that this decrease is the result of an increase in coronary flow.

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.

Movement of potassium between muscle and blood in response to respiratory acidosis

1963 ◽  
Vol 204 (5) ◽  
pp. 761-764 ◽  
Author(s):  
Roswith I. Ladé ◽  
E. B. Brown
Keyword(s):  
Skeletal Muscle ◽  
Coronary Sinus ◽  
Gastrocnemius Muscle ◽  
Respiratory Acidosis ◽  
Plasma Potassium ◽  
Blood Samples ◽  
Air Breathing ◽  
Vascular Bed ◽  
Anesthetized Dogs ◽  
Transient Elevation

Experiments have been performed on anesthetized dogs in order to study 1) the movement of potassium between the gastrocnemius muscle and blood during and following 2 hr of respiratory acidosis produced by breathing 30% CO2 in O2, and 2) the differences between skeletal and cardiac muscle with respect to potassium movement during the first 10 min of breathing CO2 and after return to air breathing. Plasma potassium concentrations were determined in blood samples drawn simultaneously from an artery and from either the vein draining the vascular bed of the skeletal muscle or the coronary sinus. It was found that skeletal muscle lost potassium during hypercapnia. The loss was evident much earlier and was greater if the muscle was stimulated to intermittent contraction than if it was resting. The heart began to gain potassium a few minutes after CO2 breathing began and lost potassium shortly after return to air breathing following 11 min of hypercapnia. There was no evidence for a contribution of skeletal muscle to the high transient elevation of the arterial potassium concentrations in the early posthypercapnic period.

Early increase of plasma potassium in hyperventilation

1965 ◽  
Vol 208 (3) ◽  
pp. 537-540 ◽  
Author(s):  
Enrique S. Blesa ◽  
Norberto C. González ◽  
Horacio E. Cingolani
Keyword(s):  
Potassium Concentration ◽  
Venous Blood ◽  
Plasma Potassium ◽  
Peripheral Venous Blood ◽  
Potassium Release ◽  
Early Increase

Plasma potassium concentration was determined in arterial and in portal, hepatic, and peripheral venous blood during acute respiratory alkalemia. It was found that passive hyperventilation produces an increase in plasma potassium, reaching peak values after 15 min. The hyperkalemia is due to potassium release in the prehepatic splanchnic territory. The liver apparently plays no part in producing it, while muscular territories take up potassium.

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.

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.

Relationship of potassium and calcium to hypothermic ventricular fibrillation

1959 ◽  
Vol 14 (1) ◽  
pp. 60-62 ◽  
Author(s):  
William R. Beavers ◽  
Benjamin G. Covino
Keyword(s):  
Ventricular Fibrillation ◽  
Potassium Chloride ◽  
Serum Calcium ◽  
Combined Therapy ◽  
Plasma Potassium ◽  
Body Temperatures ◽  
Anesthetized Dogs ◽  
Ionic Imbalance ◽  
Relationship Of ◽  
Ice Water

Pentobarbital-anesthetized dogs, cooled in ice water to terminus, were found to have a 96% incidence of ventricular fibrillation. Plasma potassium levels were uniformly depressed at low body temperatures. Treatment with Intravenous potassium chloride, 150– 250 mg/kg, reduced the frequency of fibrillation to 57%. Administration of EDTA (ethylene diamine tetracetic acid), 75 mg/kg in divided doses, lowered serum calcium levels but affected the incidence of fibrillation only slightly. Combined therapy with potassium chloride and EDTA reduced the incidence of ventricular fibrillation to 50%. These results are interpreted as indicating that ionic imbalance observed with hypothermia produces a marked arrhythmic tendency and that proper alteration of plasma potassium levels reduces the danger of fibrillation. Submitted on July 28, 1958

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.

AKTA BORGTOCHT DALAM PERJANJIAN KREDIT

2019 ◽  
Vol 5 (1) ◽  
pp. 50-61
Author(s):  
G Victor William
Keyword(s):  
Economic Interest ◽  
Standard Contract ◽  
Written Form ◽  
Relationship Of ◽  
Made In

Personal guarantee (borgtocht) is an additional agreement (accesoir) which is made for the benefit of the creditor. Personal guarantee cannot exist if there is no legal principal agreement between the creditor and the debtor, therefore this guarantee agreement involves three parties, namely the creditor, the debtor and the guarantor. The main reason for the making of personal guarantee agreement is because there is a relationship of interest between the guarantor and the debtor (the guarantor has an economic interest in the business of the debtor). Personal guarantee in practice are always made in written form. Personal guarantee agreement can be made in the form of under the hand deed or notarial deed. In banking practices, the agreement is made in the form of a standard contract that has been provided by the bank as the creditor. The party that signs this deed is the debtor and the guarantor, hereinafter the deed kept by the bank.

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