Dehydroepiandrosterone Sulfate as a Digitalis Like Factor in Plasma of Healthy Human Adults

Vasdev, Sudesh; Longerich, L; Johnson, E.; Brent, David A.; Gault, M. H.

doi:10.1016/s0022-5347(17)45809-5

Cited by 24 publications

(17 citation statements)

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“…This group has most recently suggested that dehydroepiandrosterone accounts for some of the digoxin immunoreactivity in plasma and that this steroid also is a Na + ,K + -ATPase inhibitor. 32 Further confirmation of this observation is awaited with interest. Crabos et al 33 also used HPLC to fractionate plasma and urine in normal and hypertensive subjects.…”

Section: Plasmamentioning

confidence: 83%

The search for a hypothalamic Na+,K+-ATPase inhibitor.

Haber¹,

Haupert²

1987

Hypertension

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SUMMARY Accumulating experimental evidence suggests that natrjuresis in response to intravascular volume expansion is promoted by an endogenous regulator of Na + ,K + -adenosine triphosphatase (ATPase). Efforts to purify this substance by a number of laboratories have as yet been unsuccessful. The properties of partially purified inhibitors from plasma, urine, and tissue often fall to possess the characteristics thought to be consistent with those of a physiological regulator. These include potency (K, of approximately 1 nM), reversibility of inhibition, specificity for Na + ,K + -ATPase, and responsiveness to relevant physiological stimuli. Two rather different candidate substances, extracted from urine and hypotbalamus, have been purified to a high degree. Neither is a peptide, and both are of low molecular weight and resistant to acid hydrolysis. The substance from urine is rather nonpolar and interacts with digoxin-specific antibodies, while that from hypothalamus is polar and does not appear to share epitopes with the cardiac glycosides. On the serosal surface of the toad urinary bladder, the hypothalamic substance causes a reversible inhibition of Na + transport, inhibits rubidium uptake in red blood cells by acting on the membrane's exterior surface, inhibits binding of ouabain to purified Na + ,K + -ATPase, and reversibly inhibits hydrolysis of adenosine S'-triphosphate by the enzyme with a A', of 1.4 nM. The hypothalamic inhibitor may be differentiated from ouabain by their respective ionic requirements for optimal inhibition of enzymatic activity, and although both ouabain and the hypothalamic inhibitor fix Na + ,K + -ATPase in its Ej conformation, the hypothalamic inhibitor does not promote phosphoryiation of the enzyme by inorganic phosphate in the presence of

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Section: Plasmamentioning

confidence: 83%

The search for a hypothalamic Na+,K+-ATPase inhibitor.

Haber¹,

Haupert²

1987

Hypertension

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“…Fatty acids (27,29), phospholipids (27,30), steroids (31), and bile acids (32, 33) have all been suggested äs "digoxin-like immunoreactive factors", with varying degrees of probability. "Digoxin-like immunoreactive factors" certainly represent a heterogeneous group of substances, with certain common properties and characteristics, i.e.…”

Section: Discussionmentioning

confidence: 99%

Determination of Digoxin in the Blood of Pregnant Women, Fetuses and Neonates before and during Anti-arrhythmic Therapy, Using Four Immunochemical Methods

Schlebusch

Mende²

1991

Clinical Chemistry and Laboratory Medicine

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Summary:Four immunochemical methods for digoxin assay were used to analyse control samples, 33 amniotic fluid samples, 57 samples from digitalis-treated, non-pregnant women, 90 pregnancy serum samples, and 72 samples of fetal or neonatal serum with or without digoxin therapy. One hundred and five samples were also submitted to ultrafiltration before analysis.Three methods (RIA, TD X , AMERLITE) showed practically the same precision, while the precision of the DELFIA was markedly inferior. In the analysis of serum samples from digoxin-treated, non-pregnant women, RIA and TD X gave practically the same values, whereas AMERLITE and DELFIA gave significantly higher values.Pregnancy serum and fetal serum contain "digoxin-like immunoreactive factors", and the qualitative and quantitative effects of these interfering factors are different for each of the four methods. The greatest sensitivity to "digoxin-like immunoreactive factors" is shown by TD X and DELFIA, while the lowest interference by "digoxin-like immunoreactive factors" is found in the analysis of ultrafiltered samples, using the TD X method.The composition of the "digoxin-like immunoreactive factors" in pregnancy serum and in fetal serum is altered by digoxin therapy, and these changes have different effects on the various analytical methods. The concentration of "digoxin-like immunoreactive factors" in the serum of fetuses receiving digoxin is markedly lower than that of healthy fetuses.For the reliable monitoring of digoxin therapy in the maternal and fetal circulation, the blood samples must be submitted to ültrafiltration before analysis.

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“…The plasma of salt-loaded humans and rats stimulates G6PD about 20 times more than when these species are deprived of sodium. stances, many of which are known to have metabolic effects on the proximal tubule and some of which have been demonstrated to inhibit purified preparations of Na + ,K + -ATPase, including fatty acids (linoleic and oleic), 14 '" dehydroepiandrosterone sulfate, 16 lysophosphatidyl choline, 17 and sodium vanadate. 18 None stimulated G6PD at 2 minutes.…”

Section: Discussionmentioning

confidence: 99%

Cytochemically assayable Na+,K+-ATPase inhibition by Milan hypertensive rat plasma.

Holland¹,

Millett²,

Alaghband‐Zadeh³

et al. 1987

Hypertension

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SUMMARY The ability of plasma from 3-and 9-week-old Milan hypertensive rats and their nor motensive controls to inhibit Na + ,K+-adenosine triphosphatase (ATPase) was studied using cytochemical bioassay techniques in fresh tissue. With a validated cytochemical bioassay that measures the capacity of biological samples to stimulate glucose-6-phosphate dehydrogenase activity in guinea pig proximal tubules as an indication of their capacity to inhibit Na+,K+-ATPase, the mean gIucose-6-phosphate dehydrogenase-stimulating ability of the plasma of the 9-week-old Milan hypertensive rats and their normotensive controls was 586.0 ± 88 and 23.4 ± 8.3 U/ml (n = 7; p<0.001), while that of the 3-week-old Milan hypertensive rats (before the main rise in arterial pressure) and their normotensive controls was 99.9 ± 27.4and 7.8 ± 1.8 U/ml (n = 7; p<0.001). With the use of a semiquantitative cytochemical assay that measures Na+,K+-ATPase activity directly, plasma from the adult hypertensive rats had a much greater capacity to inhibit Na + ,K+-ATPase than the plasma of the control rats. The significantly raised levels found in the young hypertensive rats before the main rise in arterial pressure are consistent with the hypothesis that the rise hi the ability of plasma to inhibit Na+,K+-ATPase is due to an inherited renal difficulty in excreting sodium. (Hypertension 9:498-503, 1987) KEY WORDS • plasma • glucose-6-phosphate dehydrogenase-stimulating activity hypertensive rats • cytochemical assay • Na + ,K+-ATPase-inhibiting activity Milan

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Dehydroepiandrosterone Sulfate as a Digitalis Like Factor in Plasma of Healthy Human Adults

Cited by 24 publications

References 0 publications

The search for a hypothalamic Na+,K+-ATPase inhibitor.

The search for a hypothalamic Na+,K+-ATPase inhibitor.

Determination of Digoxin in the Blood of Pregnant Women, Fetuses and Neonates before and during Anti-arrhythmic Therapy, Using Four Immunochemical Methods

Cytochemically assayable Na+,K+-ATPase inhibition by Milan hypertensive rat plasma.

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