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10.1159/000180516

http://scihub22266oqcxt.onion/10.1159/000180516
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1101088!ä!1101088

suck abstract from ncbi


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pmid1101088      Nephron 1975 ; 15 (3-5): 261-78
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  • Kidney and adrenocortical hormones #MMPMID1101088
  • Kleeman CR; Levi J; Better O
  • Nephron 1975[]; 15 (3-5): 261-78 PMID1101088show ga
  • We have presented a review of the interrelationship between the kidney and the adrenocortical steroids, aldosterone and cortisol primarily in the regulation of water and electrolyte metabolism. The presentation is divided into three parts: (1) the influence of cortisol and aldosterone on renal structure and function; (2) the effect of kidney disease on secretion and metabolism of these steroids, and (3) the role of the kidneys in the plasma clearance of these steroids and their metabolites. There is no evidence that an excess or deficit of these steroids have a direct effect on renal structure, but both are necessary to maintain normal GFR and RPF. Glucocorticoids augment renal hemodynamics in pharmacologic doses. The phenomenon of 'escape' by the kidney from the sodium-retaining effect of adrenocortical steroids is discussed in detail, as well as the ability of glucocorticoid to antagonize the sodium retaining activity of any adrenal steroid of analogue with lesser glucocorticoid noperties. It is included that the impaired water dunesis of glycocorticoid deficiency is due to the absence of the permissive action of these steroids on the kidney, augmented at times by enhanced ADH secretion in response to sustained nonosmotic stimuli. The effect of gluco and mineralocorticoids on the renal excretion of divalentions and uric acid is also discussed. While progressive chronic renal failure (CRF) does not seem to significantly after the secretion or metabolism of cortisol it is possible that CRF causes a state of chronic hyperaldosteronism that is essential to maintain normal excretion (secretion) of potassium per nephron as renal mass progressively decreases. A direct or an indirect effect of potassium ion may be responsible for the hypersecretion or aldosterone rather than the renin-angiotensin system.
  • |Acidosis/physiopathology[MESH]
  • |Aldosterone/pharmacology/*physiology[MESH]
  • |Animals[MESH]
  • |Calcium/metabolism[MESH]
  • |Dogs[MESH]
  • |Glomerular Filtration Rate[MESH]
  • |Glucocorticoids/physiology[MESH]
  • |Humans[MESH]
  • |Hydrocortisone/pharmacology/*physiology[MESH]
  • |Kidney Failure, Chronic/physiopathology[MESH]
  • |Kidney/blood supply/*metabolism/physiopathology[MESH]
  • |Magnesium/metabolism[MESH]
  • |Mineralocorticoids/physiology[MESH]
  • |Potassium/metabolism[MESH]
  • |Sodium/metabolism[MESH]
  • |Water-Electrolyte Balance[MESH]


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