Editing Renal Hypertension (section)

=== Pathophysiology of renal hypertension ===

* '''Two-Kidney, One-Clip Model (2K1C) i.e. vasoconstrictor hypertensive model'''
** Because of the ischemia induced by the unilateral stenosis, '''renin secretion is increased from the juxtaglomerular apparatus of the ischemic kidney and suppressed in the normal contralateral kidney.'''
** '''As a consequence of the activation of the renin-angiotensin-aldosterone system (RAAS''') '''and an increased production of angiotensin II, there is peripheral vasoconstriction and hypertension'''
** '''This form of hypertension may be managed with (3):'''
**# '''Reversal of the RAAS (or unclipping of the “clipped kidney”)'''
**# '''ACE inhibitors'''
**# '''Angiotensin receptor blockade'''
* '''One-Kidney, One-Clip (1K1C) Model i.e. volume hypertensive model'''
** There is '''[an initial] activation of the RAAS''' similar to that seen in the 2K1C model. However, in contrast to the 2K1C kidney, '''the absence of a normal contralateral kidney prevents an ensuing natriuresis and diuresis. Thus, there is''' '''volume expansion, and renin secretion is suppressed in the clipped kidney''' because of feedback inhibition. Volume expansion remains, and there is '''sustained hypertension in spite of the decreased vasoconstriction''' associated with the now '''suppressed RAAS.'''
** '''1K1C model is driven by volume expansion and sodium retention with normal circulating levels of angiotensin II.'''