AVP and inappropriate ADH syndrome: Angiotensin II, via its receptors on the third ventricle floor, directly stimulates ADH release into the ventricle via baroreception [21] or hypothalamic supraoptic nucleus damage [22]. The elevation of plasma ALA and PBG levels is definitively the trigger for acute attacks in hepatic porphyrias; however, hyponatremia and the development of SIADH are critical factors influencing patient prognosis [21].