Circulatory and vestibular implications of central angiotensin mechanisms in physiological adaptation to weightlessness.
The discovery of an iso-renin angiotensin (AII) system within the central nervous system (CNS) led investigators to theorize a physiological and/or pathological role for the central actions of AII. Activation of central AII receptors in specific brain regions elicits antidiuretic, dipsogenic and pressor responses subsequently producing net body fluid retention. Removal of hydrostatic forces during weightlessness causes a massive translocation of body fluids to the thoraco-abdominal region; physiological adaptation to such a change is manifested as adipsia and net body fluid loss. It is suggested that these events may result from a decrease in the CNS-mediated effects of AII due to suppression of circulating AII levels. Depressed AII activity in the area postrema (AP) may also be responsible for the atypical nausea characteristic of space sickness.
D000222:Adaptation, Physiological; D000804:Angiotensin II / Q000097:blood / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000502:physiology*; D004285:Dogs; D004723:Endorphins / Q000502:physiology; D006801:Humans; D008526:Medulla Oblongata / Q000503:physiopathology; D009292:Narcotic Antagonists / Q000627:therapeutic use; D009325:Nausea / Q000188:drug therapy / Q000503:physiopathology; D051381:Rats; D013026:Space Flight; D014893:Weightlessness
D004723:Endorphins; D009292:Narcotic Antagonists; D000804:Angiotensin II