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Taking corticosteroids can result in high blood pressure.

Is anything known about the physiological mechanism behind this? Why do corticosteroids have this side effect?

Since it's been mentioned in the comments, the Wikipedia article includes a section reading

Corticosteroids can cause sodium retention through a direct action on the kidney, in a manner analogous to the mineralocorticoid aldosterone. This can result in fluid retention and hypertension

But does not cite any sources for that section at all. Neither does the article on aldosterone.

  • en.wikipedia.org/wiki/Corticosteroid "Corticosteroids can cause sodium retention through a direct action on the kidney, in a manner analogous to the mineralocorticoid aldosterone. This can result in fluid retention and hypertension." – Count Iblis Dec 25 '15 at 15:07
  • @CountIblis there are two mentions of hypertension in the Wikipedia article - both seem to cite no sources whatsoever (the article is marked as lacking citations) – YviDe Dec 25 '15 at 15:14
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I've found a supporting source for the fluid retention claim, in an excerpt from Holland-Frei Cancer Medicine, 6th edition (from 2003). This separates the effects on the kidney into two categories, depending in part on the drug: mineralocorticoid and glucocorticoid.

Mineralocorticoid effects include

  • Loss of potassium and hydrogen
  • Increase in extracellular fluid volume
  • Increase in sodium retention

Glucocorticoid effects include

  • Increase in plasma flow in the kidney
  • Increase in sodium retention

Both types of effects can occur in limited frequencies outside the kidney, generally in the gastrointestinal system.


These effects can then lead to a variety of symptoms, including high blood pressure. Mineralocorticoids can cause chronic arterial hypertension through long-term sodium retention. Glucocorticoids can do the same, through several factors (the details of which are unknown):

  • Increase in filtration fraction, the ratio of glomerular filtration rate to renal plasma flow[1]
  • Increase in glomerular hypertension, high pressure in the glomerular capillaries[2]
  • Increase in synthesis of angiotensinogen, a protein involved in regulating blood pressure,[3] and atrial natriuretic peptide[4], a peptide involved in regulating renal blood flow and sodium excretion
  • Decrease in the synthesis of prostaglandin, lipids that in the kidney regulate blood flow and vasodilation[5]
  • Increase in vasopressor responsiveness (interestingly enough, this can be related to angiotensin II; see Drury et al. (1984))

Vasodilation refers to the size of the capillaries; dilation of the capillaries decreases blood pressure, while the reverse increases blood pressure. This is perhaps the most direct effect of corticosteroids on hypertension and blood pressure.

Note: Here, the superscripts indicate secondary sources that explained the significances of these in more detail (which I included); the textbook merely listed them.


Additional sources cited:

[1]: Costnazo, Linda. Physiology: Cases and Problems
[2]: Juan Macías-Núñez et al. The Aging Kidney in Health and Disease
[3]: AGT angiotensinogen (serpin peptidase inhibitor, clade A, member 8) [ Homo sapiens (human) ]
[4]: Claudio Ronco et al. Critical Care Nephorology
[5]: Jasjit Bindra. Prostaglandin Synthesis

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