Evidence for a dual central role for angiotensin in water and sodium intake

Abstract

ANGIOTENSIN II induces short-latency water intake when infused intravascularly or injected into certain brain regions of mammals^1,2. But conceptual difficulties arise if one asks why this should be so, and whether the data reflect real physiological actions. For example, angiotensin is a pressor hormone formed from kidney-based renin in response to challenge such as hypotension and hypovolaemia^3–7. Water ingestion, in itself, is not an adaptive response to such challenges, since most ingested water is distributed intracellularly and will not relieve a vascular crisis. An adaptive response to hypotension or hypovolaemia would involve ingestion of an isotonic mix of fluids, since this would most rapidly and effectively increase vascular volume. In fact, hypovolaemia does result in an immediate increase in preference for isotonic saline over water and a delayed (6–10 h) acceptance of unpalatable hypertonic salt solutions^8,9. But, a possible involvement of angiotensin as a rapid and direct facilitator of sodium intake (apart from a slow and indirect role through stimulation of aldosterone release) has not yet been reported and some evidence suggests that angiotensin may not play any significant role in regulating sodium intake in the rat^10–12.