Physiological and pathophysiological actions of the main angiotensin II degradation products in the brain tissue

Degradation products	Action	Source
AT 1-7	Participating in the implementation of learning and memorization	[1, 51]
	Preventing the norepinephrine release, increasing the local production of bradykinin and nitric oxide Stimulation of vasopressin secretion	[43]
	Regulation of vascular tone, cell proliferation, inflammation	[48]
	Protection of NVU cells in insulin resistance, cardiovascular and renal diseases	[49, 50]
	Reducing anxiety Modifying the production of corticotropin-releasing hormone in the hypothalamus	[52]
	Decreasing the production of free radicals Initiation of redox signal transduction	[53]
	Modifying the expression of tight junction proteins (claudin-5, ZO1) Reducing the expression of matrix metalloproteinase MMP-9 Stimulation of ATP production Preventing mitochondrial fragmentation	[54, 55] [56]
AT IV	Protecting brain cells from ischemia, reducing memory deficit	[49, 50, 57, 58]
	Inhibiting the catalytic activity of IRAP Modifying the glucose transport into cells	[59]
	Inhibition of cysteine aminopeptidase (improving learning and memorization) Anticonvulsant and antiepileptic action Control over the cerebral vascular tone	[59, 60]
	Accumulation of endogenous oxytocin	[61]