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During the time of long-term administration of diuretics such as frusemide (a potent "loop" diuretic, which acts on the ascending limb of the loop of Henle), and particularly where the initial indication for such therapy was not strong, a depletion of body sodium may occur to levels below normal. In this situation, a secondary (compensatory) release of renin occurs from the juxtaglomerular apparatus (JGA) and, via angiotensin II production, stimulates the release of aldosterone to limit sodium (E.C.F. volume) loss. Now in the early stages, this stimulated renin release is rapidly reversible on withdrawal of the diuretic concerned. However after months or years the juxtaglomerular apparatus undergoes hyperplasia, which may eventually become relatively autonomous, so that when the diuretics are withdrawn, there may be marked fluid retention due to continued autonomous activity of the renin-angiotensin-aldosterone system.
Explanation: Angiotensine II is vasodilatatory which means it widens the blood vessels. This is secondary (in the sense of helping) to the liberation of the kidney, i.e. it helps the flow in the Glomeruli going.