What is the physiological mechanism behind the occurrence of orthostatic hypertension in the presence of hypovolemia?

  • $\begingroup$ it would really be helpful if you could like to some external references for terms like this :) $\endgroup$
    – shigeta
    May 25, 2014 at 4:06
  • $\begingroup$ Orthostatic (=postural) hypertension is an excessive increase of blood pressure upon standing up. Hypovolemia is a reduced total blood volume (i.e. lack of plasma). This question is perfectly on-topic. $\endgroup$
    – Armatus
    May 25, 2014 at 11:50

2 Answers 2


The pathophysiology of orthostatic hypertension has not been elucidated. It is believed it involves activation of the sympathetic nervous system [1], vascular adrenergic hypersensitivity and diabetic neuropathy [2]. High levels of plasma atrial natriuretic peptide and antidiuretic hormone were observed in children [3].

Hypovolemia causes:

  • baroreflex-mediated increase in muscle sympathetic nerve activity [4]
  • release of epinephrine and norepinephrine [5]
  • activation of renin-angiotensin axis [5], thus increasing ADH levels

All these reactions result in vasoconstriction and blood pressure raising. But not up to absolute hypertension.

Orthostatic hypertension is diagnosed by a rise in systolic blood pressure of 20 mmHg or more when standing [6].

This is possible. A raise of 20 mmHg from hypotension could result due to vasoconstriction.


  1. Fessel J, Robertson D. Orthostatic hypertension: when pressor reflexes overcompensate. Nat Clin Pract Nephrol. 2006 Aug;2(8):424-31. doi: 10.1038/ncpneph0228. PubMed PMID: 16932477.

  2. Chhabra L, Spodick DH. Orthostatic hypertension: recognizing an underappreciated clinical condition. Indian Heart J. 2013 Jul 5;65(4):454-6. doi: 10.1016/j.ihj.2013.06.023. PubMed PMID: 23993009.

  3. Zhao J, Yang J, Du S, Tang C, Du J, Jin H. Changes of atrial natriuretic peptide and antidiuretic hormone in children with postural tachycardia syndrome and orthostatic hypertension: a case control study. Chin. Med. J. 2014 May;127(10):1853-7. PubMed PMID: 24824244.

  4. Ryan KL, Rickards CA, Hinojosa-Laborde C, Cooke WH, Convertino VA. Sympathetic responses to central hypovolemia: new insights from microneurographic recordings. Front Physiol. 2012 Apr 26;3:110. doi: 10.3389/fphys.2012.00110. PubMed PMID: 22557974.

  5. Wikipedia contributors, "Shock (circulatory)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Shock_(circulatory)&oldid=612494727 (accessed June 26, 2014).

  6. Wikipedia contributors, "Orthostatic hypertension," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Orthostatic_hypertension&oldid=603984647 (accessed June 26, 2014).


I presumed you meant orthostatic hypotension.

Blood pressure falls on standing and is caused primarily by increased gravity causing blood pooling in the legs. This reduces venous return and subsequently cardiac output and therefore arterial blood pressure. Usually however standing doesn't usually cause a massive fall in blood pressure as standing immediately triggers vasoconstriction (baroreceptor reflex), pressing the blood up into the body again. However when there's a secondary factor reducing blood pressure such as hypovolaemia, the fall in pressure is higher than the body may sometimes be able to compensate for. This causes symptomatic orthostatic hypotension.

  • $\begingroup$ No I meant orthostatic hypertension, which apparently can also a symptom of hypovolemia. For instance, look at the 5th cause on the list on wikipedia en.wikipedia.org/wiki/Orthostatic_hypertension. $\endgroup$
    – Kenshin
    Feb 27, 2014 at 7:52
  • $\begingroup$ Ah okay. Orthostatic hypertension: Sometimes the above mechanism can overdo it in whats thought to be through an alpha adrenergic system. This is rare and medical communities doubt its existence. $\endgroup$ Feb 27, 2014 at 7:56

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