Collective experimental and clinical evidence demonstrates that: i) the CSF titer of ANP increases proportionally to CSFP elevation [98], ii) the CSF level of ANP is elevated in high-pressure hydrocephalus [99,100], iii) the ANP receptors in CP undergo a Vmax adjustment to compensate for the CSFP increase in hydrocephalus [88,101], and iv) the CPe is bioreactive to ANP [82] and modulates CSF formation [102] by a cGMP-dependent mechanism [86,103]. Here, NPPA is linked to Hydrocephalus.