Studies on two novel angiotensin II actions.
Animal data suggest that angiotensin II may directly affect renal sodium retention independent of aldosterone (4,6). Additionally there is evidence to suggest that the hormone can stimulate protein synthesis in a variety of tissues and that indeed it may be a vasculotoxin (5,7). We describe here experiments designed to elucidate the role of angiotensin II in renal sodium retention in normal man. Additionally we present preliminary evidence suggesting that unlike the rapid sodium retaining effect, some delayed (trophic) actions of the hormone may be generated by a hitherto unappreciated mechanism.
D000328:Adult; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight; D002467:Cell Nucleus / Q000378:metabolism; D004039:Diet, Sodium-Restricted; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D009842:Oligopeptides; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D012083:Renin / Q000097:blood*; D013722:Teprotide
D009842:Oligopeptides; D000804:Angiotensin II; D000450:Aldosterone; D013722:Teprotide; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D006854:Hydrocortisone