In rats with acute hypo- and hyperglycemia the initial effects of free angiotensin IV and its complexes with functionally different carrier proteins (transport protein BSA, neuron-specific protein S100b) on hemodynamics and behavior of rats were qualitatively altered, in comparison with those in intact animals. At the same time, free angiotensin IV under conditions of hypo- and hyperglycemia paradoxically acquired functions of angiotensin II (moderate hypertension, tachycardia, polydipsia and activation of instrumental drinking behavior). Concurrently, complexes of angiotensin IV with BSA and S100b acquired functions of free angiotensin IV (hypotensia, suppression of drinking behavior). It is suggested that complexes of angiotensin IV with functionally different proteins are involved in a differentiated way first in compensation of behavior and hemodynamics impairment produced by acute and/or chronic hypo- and hyperglycemia, and then in qualitative transformation of these adaptive processes into stable pathological condition involving mechanisms of so called "metabolic memory".