Effect of hydrogen ion concentration on aldosterone secretion by isolated perfused canine adrenal glands

1986 ◽  
Vol 110 (2) ◽  
pp. 293-301 ◽  
Author(s):  
K. J. Radke ◽  
R. E. Taylor ◽  
E. G. Schneider
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Glands ◽  
Recovery Period ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Aldosterone Secretion ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Secretory Rate

ABSTRACT The direct effects of changes in extracellular hydrogen ion (H+) concentration on aldosterone secretion under basal, angiotensin II- and potassium-stimulated conditions were studied in isolated, perfused canine adrenal glands. Changes in extracellular H+ concentration were induced by altering either the partial pressure of CO2 (pCO2) or the HCO3− concentration of the perfusate. Acid-base disturbances had a more pronounced effect on aldosterone secretion under stimulated than under basal conditions. Increasing H+ concentration enhanced angiotensin II- and potassium-stimulated aldosterone secretion, whereas decreasing H+ concentration markedly inhibited the secretory response to these stimuli. Because changes in H+ concentration, whether produced by varying extracellular pCO2 or extracellular HCO3− concentration, had similar effects on angiotensin II-stimulated aldosterone secretion, the data suggest that H+ concentration per se is the important determinant of the aldosterone secretory rate. Interestingly, during the immediate recovery period from pCO2-induced alkalosis under both angiotensin II- and potassium-stimulated conditions, aldosterone secretion always returned to a value significantly higher than that obtained just before alkalosis. The results of this study demonstrate that changes in extracellular H+ concentration influence the rate of aldosterone secretion, possibly via changes in intracellular pH, by a direct action on the canine adrenal gland. Therefore, when evaluating the control of aldosterone secretion, the acid-base status of the whole animal or of in-vitro adrenal tissue must be considered. J. Endocr. (1986) 110, 293–301

Effect of hydrogen ion concentration on corticosteroid secretion

1986 ◽  
Vol 250 (3) ◽  
pp. E259-E264 ◽  
Author(s):  
K. J. Radke ◽  
E. G. Schneider ◽  
R. E. Taylor ◽  
R. E. Kramer
Keyword(s):  
Adrenal Glands ◽  
Direct Action ◽  
Zona Glomerulosa ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Direct Effects ◽  
Aldosterone Secretion ◽  
Hydrogen Ion Concentration ◽  
Significant Direct Effect ◽  
Corticosteroid Secretion

The direct effects of changes in extracellular hydrogen ion (H+) concentration on corticosteroid secretion under basal and ACTH-stimulated conditions were studied in isolated, perfused canine adrenal glands. Changes in extracellular H+ concentration were produced by altering either PCO2 or [HCO-3] of the Krebs-bicarbonate perfusate. Alkalosis markedly inhibited ACTH-stimulated aldosterone secretion. Moreover, within the range of pH from 7.19 to 7.85, there was a positive correlation between H+ concentration and the fractional secretion of aldosterone but a negative correlation between H+ concentration and the fractional secretion of corticosterone and 18-hydroxycorticosterone in response to ACTH. In contrast, neither acidosis nor alkalosis had a significant, direct effect on basal or ACTH-stimulated cortisol secretion. We conclude that 1) H+ concentration modulates the stimulatory effect of ACTH on aldosterone secretion by a direct action on the adrenal cortex, 2) acid-base disturbances are specific to the zona glomerulosa of the canine adrenal gland, and 3) H+ concentration may influence events occurring late in the pathway for aldosterone biosynthesis.

ACID-BASE LANGUAGE VERSUS ACID-BASE MEASUREMENTS

PEDIATRICS ◽  
1969 ◽  
Vol 43 (5) ◽  
pp. 830-832
Author(s):  
Giles F. Filley
Keyword(s):  
The Body ◽  
Ion Concentration ◽  
Volatile Acid ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Base Language ◽  
Physicochemical System ◽  
American Schools ◽  
Anglo American

The PAPERS of Kildeberg and Engel and of Nelson and Riegel continue what has been called, inaccurately, "The Great Transatlantic Acid-Base Debate" betsveen two schools of acid-base physiology. Historically at least, these can be called the Continental and Anglo-American Schools and their current dispute a war of words. We will sketch their beginnings, describe some of their differences, and indicate the importance of the distinction between fundamental and derived measurement. The Continental School was probably founded by Hasselbalch, who in 1916 began the apparently never-ending search for a chemical index of a "metabolic component," i.e., a number indicating the quantity of non-volatile acid added to or lost from the body-"corrected" for respiratory effects. Hasselbalch index was typical of the genre because it required exposing a blood specimen in vitro to known CO2 gas mixtures and was called a "reduced hydrogen ion concentration." His successors have tended to work meticulously in chemical laboratories, to give special names to defined magnitudes, and to incorporate these into logical formulations. One example was that of Singer and Hastings, which was based on a thoroughgoing study of blood as a physicochemical system at various states of equilibrium outside the body. Another recent and carefully developed one is that of Siggaard-Andersen. Despite this and other authors warnings, this school formulations are subject to abuse perhaps especially by those who assume that an "Astrup determination" is a substitute for clinical judgement. The other school is less systematic, its members being more often physiologists or physicians than physical chemists.

A physiological approach to acid–base disorders: The roles of ion transport and body fluid compartments

2020 ◽  
pp. 2182-2198
Author(s):  
Julian Seifter
Keyword(s):  
Metabolic Acidosis ◽  
Gas Analysis ◽  
Hydrogen Ion ◽  
Anion Gap ◽  
Ion Concentration ◽  
Hydrogen Ions ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood Gas ◽  
Fluid Compartments

The normal pH of human extracellular fluid is maintained within the range of 7.35 to 7.45. The four main types of acid–base disorders can be defined by the relationship between the three variables, pH, Pco2, and HCO3 –. Respiratory disturbances begin with an increase or decrease in pulmonary carbon dioxide clearance which—through a shift in the equilibrium between CO2, H2O, and HCO3 –—favours a decreased hydrogen ion concentration (respiratory alkalosis) or an increased hydrogen ion concentration (respiratory acidosis) respectively. Metabolic acidosis may result when hydrogen ions are added with a nonbicarbonate anion, A−, in the form of HA, in which case bicarbonate is consumed, or when bicarbonate is removed as the sodium or potassium salt, increasing hydrogen ion concentration. Metabolic alkalosis is caused by removal of hydrogen ions or addition of bicarbonate. Laboratory tests usually performed in pursuit of diagnosis, aside from arterial blood gas analysis, include a basic metabolic profile with electrolytes (sodium, potassium, chloride, bicarbonate), blood urea nitrogen, and creatinine. Calculation of the serum anion gap, which is determined by subtracting the sum of chloride and bicarbonate from the serum sodium concentration, is useful. The normal value is 10 to 12 mEq/litre. An elevated value is diagnostic of metabolic acidosis, helpful in the differential diagnosis of the specific metabolic acidosis, and useful in determining the presence of a mixed metabolic disturbance. Acid–base disorders can be associated with (1) transport processes across epithelial cells lining transcellular spaces in the kidney, gastrointestinal tract, and skin; (2) transport of acid anions from intracellular to extracellular spaces—anion gap acidosis; and (3) intake.

scholarly journals SOME CONSEQUENCES OF THE THEORY OF MEMBRANE EQUILIBRIA

1925 ◽  
Vol 9 (1) ◽  
pp. 97-109 ◽  
Author(s):  
David I. Hitchcock
Keyword(s):  
Membrane Potential ◽  
Osmotic Pressure ◽  
Ionization Constant ◽  
Weak Acid ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Weak Base ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Pass Through

In applying Donnan's theory of membrane equilibria to systems where the non-diffusible ion is furnished by a weak acid, base, or ampholyte, certain new relations have been derived. Equations have been deduced which give the ion ratio and the apparent osmotic pressure as functions of the concentration and ionization constant of the weak electrolyte, and of the hydrogen ion concentration in its solution. The conditions for maximum values of these two properties have been formulated. It is pointed out that the progressive addition of acid to a system containing a non-diffusible weak base should not cause the value of the membrane potential to rise, pass through a maximum, and fall, but should only cause it to diminish. It is shown that the theory predicts slight differences in the effect of salts on the ion ratio in such systems, the effect increasing with the valence of the cation.

Effect of norepinephrine on myocardial intracellular hydrogen ion concentration

1975 ◽  
Vol 229 (2) ◽  
pp. 344-349 ◽  
Author(s):  
KM Riegle ◽  
RL Clancy
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Beta Blockade ◽  
Hydrogen Ion Concentration ◽  
Rat Hearts ◽  
Buffer Value

The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.

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