ADH is synthesized in the supra-optic and paraventricular nuclei of the hypothalamus and it is transported along axons to the posterior pituitary where it is stored . Aldosterone and vasopressin together control the handling of sodium and water . Dehydration or water deficit decreases plasma volume, renal flow and GFR . During dehydration the decrease in renal flow stimulates the renin-angiotensin-aldosterone system (RAAS)  . RAAS begins when the juxtaglomerular granular cells, under the stimulation of low blood pressure, secretes renin, an enzyme that converts inactive plasma protein angiotensinogen into angiotensin I (ANG I) . In the blood system, angiotensin-converting enzyme (ACE) converts ANG I into ANG II . ANG II will then stimulate the adrenal cortex, to synthesize and release aldosterone .
Aldosterone diffuses into the P cells and combines with its cytoplasmic receptors. The hormone-receptor complex enters nucleus to initiate the transcription of mRNA, which will now move back into the cytoplasm to the RER, where it will initiate the translation and synthesis of AIPs . AIPs modify the existing carrier proteins resulting in increased Na+ reabsorption , therefore inhibiting urinary sodium excretion . Sodium retention does not directly raise low blood pressure , but it increases plasma (ECF) osmolality  , which stimulates thirst  and vasopressin secretion from the posterior pituitary gland .
Vasopressin binds its V2 receptor , located on the basolateral  membranes of tubular cells in the collecting ducts  . Binding activates a G-protein/cAMP secondary messenger system  which in return activates protein kinase A (PKA) . PKA phosphorylates aquaporin 2 (AQP2) , causing it to move to the apical membrane and fuse with it  . Exocytosis inserts the aquaporin 2 water pores into the apical membrane , therefore increasing the cell membrane’s permeability to water  and water...
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