Abstract
Angiotensin II is as potent a stimulus for drinking in pigeons as it is in mammals. There are striking similarities in the action of this peptide in pigeons and mammals. Angiotensin II injected intracranially, i.v. or i.p. consistently caused short-latency and vigorous drinking in pigeons but no other behavior. Drinking was completed rapidly and intakes were very large, sometimes in excess of 10% of the bird''s body weight. The latency to drink and the amount drunk were dose dependent for all routes of injection. Angiotensin II was most effective when injected directly into the brain. As little as 10-14 mol angiotensin II injected into the cerebral ventricles caused birds to drink. The rapid cessation of drinking after intracranial injection of angiotensin II was not caused by rapid loss of activity of the peptide in the brain but by the actual ingestion of the water. The brain sites most sensitive to the dipsogenic action of angiotensin II in the pigeon were the dorsal and ventral third ventricle, the tissue adjacent and anterior to these sites, and the lateral ventricles. The lateral hypothalamic area was only slightly less sensitive. Negative sites for drinking were found in the lateral forebrain and the hind brain. These findings are similar to those in mammals. Pigeons drank during i.v. infusion of as little as 16 .times. 10-12 mol angiotensin II kg-1 min-1. This was near the threshold for increasing arterial pressure in pigeons and is near the threshold for drinking in rats and dogs. The Asn1, Asp1, Val5 and Ile5 analogs of angiotensin II were equipotent as stimuli to drink but a wide range of other peptides and drugs injected into the brain failed to increase water intake. An exception was eledoisin which was molecule for molecule, only 10-100 times less potent than angiotensin II in the pigeon. Injections of angiotensin II into brain sites which caused drinking failed to alter heart rate or arterial pressure in pigeons. Together with other recent studies this demonstrates the wide phylogenetic distribution of the dipsogenic action of angiotensin II; the idea that the control of water intake is an important physiological function of the renin-angiotensin system in vertebrates is supported.