What is the physiological mechanism behind the occurrence of orthostatic hypertension in the presence of hypovolemia?
The pathophysiology of orthostatic hypertension has not been elucidated. It is believed it involves activation of the sympathetic nervous system , vascular adrenergic hypersensitivity and diabetic neuropathy . High levels of plasma atrial natriuretic peptide and antidiuretic hormone were observed in children .
- baroreflex-mediated increase in muscle sympathetic nerve activity 
- release of epinephrine and norepinephrine 
- activation of renin-angiotensin axis , 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 .
This is possible. A raise of 20 mmHg from hypotension could result due to vasoconstriction.
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Wikipedia contributors, "Shock (circulatory)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Shock_(circulatory)&oldid=612494727 (accessed June 26, 2014).
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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.