Suggesting I'm a low A/BNP, high Vasopressin state: hypertension, arterial vasoconstriction, concentrated urine, hypokalemia, high pair bonding, dilated cardio hypertrophy. Low eGFR. Vasopressin associates with stress. Don't sweat. Sympathetic failure. Blurry vision, intraocular control. Na excretion plus sympathetic control is required for sweating.
Vasopressin is reacting to high ECM osmolarity. Activating aquaporin channels for diH2O outflow, attempting to deconcentrate ECM interstitial spaces. Saline provides symptom improvement. Dex, B adrenergic, sympathetic activation improves symptoms. Missing ANP energy metabolic regulation?
It kind of seems vasopressin is a cell flush and rebuild (anabolic, rest and digest program) mechanism allowing high pressure free osmotic flow compensation for permissive active transport. This theoretically would suppress high frequency passive channel signaling (ion signaling, thus especially cognition) due to prevention of high substrate osmotic gradients. If so, perhaps intracellular dysregulated/infected/stress would rapidly cause a UPR/ISR, then perhaps a synucleinopathy or taupathy, which rapidly cause intracellular hyperosmolor trash build up, especially upon exertion, which quickly activate H2O influx and cognition/sympathetic shutdown, the trash and damage activate PRRs activating an amplified and prolonged immune response and high intracellular swelling, and thus prolonged and deep cognition signaling suppression (drowsy, stupor, sleep, coma). Perhaps then excessive deregulation and repair causing excess sympathetic shutdown then causes sympathetic drive failure and is causal explanation for: central sleep apnea, ataxia, reward circuit, PFC impairment, anxiety, disassociation/schizophrenia, BPD, fear, thought disorder, ocular ataxia, inability to sweat, hypothalamic-brainstem homeostatic control, POTS, immune deficiency (huge because this is your repair system)
