Escape from the sodium-retaining effects of mineralocorticoids

F. G. Knox, John C Jr. Burnett, D. E. Kohan, W. S. Spielman, J. C. Strand

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

In our opinion, it is unlikely that a single factor mediates escape. Interruption of a single system, as repeatedly demonstrated in this review, does not prevent escape, probably due to activation of other mechanisms. For this reason, the evidence does not firmly rule out the participation of many of the individual mechanisms discussed in this review. Most likely, an interplay of several compensatory mechanisms mediates escape from the salt-retaining effect of mineralocorticoids. As stated by Smith, 'where multiple controls are super-imposed on a function, such as sodium excretion, it is conceived that normal regulatory mechanisms may be obscured by compensatory reactions'. The mechanism for escape from the salt-retaining effects of mineralocorticoids is not proven. In consideration of all of the foregoing, our current view of the mechanism for escape is as follows: Salt and water retention leads to expansion of an effective vascular volume, stimulation of volume receptors, and subsequent decreases in renal adrenergic activity. This decreased renal adrenergic activity directly decreases sodium transport as well as vasodilates the kidney, allowing increased transmission of systemic blood pressure to the renal vasculature. These factors, perhaps modulated by intrarenal hormones, increase sodium excretion and thereby mediate the escape from the salt-retaining effects of mineralocorticoids.

Original languageEnglish (US)
Pages (from-to)263-276
Number of pages14
JournalKidney International
Volume17
Issue number3
StatePublished - 1980

Fingerprint

Mineralocorticoids
Salts
Sodium
Kidney
Adrenergic Agents
Blood Vessels
Hormones
Blood Pressure
Water

ASJC Scopus subject areas

  • Nephrology

Cite this

Knox, F. G., Burnett, J. C. J., Kohan, D. E., Spielman, W. S., & Strand, J. C. (1980). Escape from the sodium-retaining effects of mineralocorticoids. Kidney International, 17(3), 263-276.

Escape from the sodium-retaining effects of mineralocorticoids. / Knox, F. G.; Burnett, John C Jr.; Kohan, D. E.; Spielman, W. S.; Strand, J. C.

In: Kidney International, Vol. 17, No. 3, 1980, p. 263-276.

Research output: Contribution to journalArticle

Knox, FG, Burnett, JCJ, Kohan, DE, Spielman, WS & Strand, JC 1980, 'Escape from the sodium-retaining effects of mineralocorticoids', Kidney International, vol. 17, no. 3, pp. 263-276.
Knox FG, Burnett JCJ, Kohan DE, Spielman WS, Strand JC. Escape from the sodium-retaining effects of mineralocorticoids. Kidney International. 1980;17(3):263-276.
Knox, F. G. ; Burnett, John C Jr. ; Kohan, D. E. ; Spielman, W. S. ; Strand, J. C. / Escape from the sodium-retaining effects of mineralocorticoids. In: Kidney International. 1980 ; Vol. 17, No. 3. pp. 263-276.
@article{df1baff059524b9ba1f75d9082d6feaf,
title = "Escape from the sodium-retaining effects of mineralocorticoids",
abstract = "In our opinion, it is unlikely that a single factor mediates escape. Interruption of a single system, as repeatedly demonstrated in this review, does not prevent escape, probably due to activation of other mechanisms. For this reason, the evidence does not firmly rule out the participation of many of the individual mechanisms discussed in this review. Most likely, an interplay of several compensatory mechanisms mediates escape from the salt-retaining effect of mineralocorticoids. As stated by Smith, 'where multiple controls are super-imposed on a function, such as sodium excretion, it is conceived that normal regulatory mechanisms may be obscured by compensatory reactions'. The mechanism for escape from the salt-retaining effects of mineralocorticoids is not proven. In consideration of all of the foregoing, our current view of the mechanism for escape is as follows: Salt and water retention leads to expansion of an effective vascular volume, stimulation of volume receptors, and subsequent decreases in renal adrenergic activity. This decreased renal adrenergic activity directly decreases sodium transport as well as vasodilates the kidney, allowing increased transmission of systemic blood pressure to the renal vasculature. These factors, perhaps modulated by intrarenal hormones, increase sodium excretion and thereby mediate the escape from the salt-retaining effects of mineralocorticoids.",
author = "Knox, {F. G.} and Burnett, {John C Jr.} and Kohan, {D. E.} and Spielman, {W. S.} and Strand, {J. C.}",
year = "1980",
language = "English (US)",
volume = "17",
pages = "263--276",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "3",

}

TY - JOUR

T1 - Escape from the sodium-retaining effects of mineralocorticoids

AU - Knox, F. G.

AU - Burnett, John C Jr.

AU - Kohan, D. E.

AU - Spielman, W. S.

AU - Strand, J. C.

PY - 1980

Y1 - 1980

N2 - In our opinion, it is unlikely that a single factor mediates escape. Interruption of a single system, as repeatedly demonstrated in this review, does not prevent escape, probably due to activation of other mechanisms. For this reason, the evidence does not firmly rule out the participation of many of the individual mechanisms discussed in this review. Most likely, an interplay of several compensatory mechanisms mediates escape from the salt-retaining effect of mineralocorticoids. As stated by Smith, 'where multiple controls are super-imposed on a function, such as sodium excretion, it is conceived that normal regulatory mechanisms may be obscured by compensatory reactions'. The mechanism for escape from the salt-retaining effects of mineralocorticoids is not proven. In consideration of all of the foregoing, our current view of the mechanism for escape is as follows: Salt and water retention leads to expansion of an effective vascular volume, stimulation of volume receptors, and subsequent decreases in renal adrenergic activity. This decreased renal adrenergic activity directly decreases sodium transport as well as vasodilates the kidney, allowing increased transmission of systemic blood pressure to the renal vasculature. These factors, perhaps modulated by intrarenal hormones, increase sodium excretion and thereby mediate the escape from the salt-retaining effects of mineralocorticoids.

AB - In our opinion, it is unlikely that a single factor mediates escape. Interruption of a single system, as repeatedly demonstrated in this review, does not prevent escape, probably due to activation of other mechanisms. For this reason, the evidence does not firmly rule out the participation of many of the individual mechanisms discussed in this review. Most likely, an interplay of several compensatory mechanisms mediates escape from the salt-retaining effect of mineralocorticoids. As stated by Smith, 'where multiple controls are super-imposed on a function, such as sodium excretion, it is conceived that normal regulatory mechanisms may be obscured by compensatory reactions'. The mechanism for escape from the salt-retaining effects of mineralocorticoids is not proven. In consideration of all of the foregoing, our current view of the mechanism for escape is as follows: Salt and water retention leads to expansion of an effective vascular volume, stimulation of volume receptors, and subsequent decreases in renal adrenergic activity. This decreased renal adrenergic activity directly decreases sodium transport as well as vasodilates the kidney, allowing increased transmission of systemic blood pressure to the renal vasculature. These factors, perhaps modulated by intrarenal hormones, increase sodium excretion and thereby mediate the escape from the salt-retaining effects of mineralocorticoids.

UR - http://www.scopus.com/inward/record.url?scp=0018858922&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018858922&partnerID=8YFLogxK

M3 - Article

C2 - 6995687

AN - SCOPUS:0018858922

VL - 17

SP - 263

EP - 276

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 3

ER -