Effects of Centrally Administered Angiotensin II on Salt and Water Excretion

Adult male rats (n = 34) acclimated to metabolism cages received 5 µl artificial cerebrospinal fluid (CSF) with or without 0.5 µg angiotensin intraventricularly (IVT). Urinary volume, Potassium excretion sodium and potassium were followed for 3 h. With a suitable recovery time between experiments every rat was randomly exposed to each of 3 test procedures and thus participated in both control and experimental conditions. The procedures consisted of (1) administration of CSF IVT after gentle bladder massage and of 5 ml water by stomach tube – CSF-PO group; (2) same, except angiotensin was injected IVT – ANG-PO group; (3) same as the ANG-PO group except the stomach tube insertion was a sham procedure; the rats were allowed to drink 5 ml water in response to angiotensin – ANG-SPON group. The angiotensin-induced drinking of 5 ml water took 5–10 min. Except for the 5 ml allowed ANG-SPON rats, water was withheld from all groups during the 3-hour experimental period, and spontaneously voided urine was collected every 15 min. The results of these experiments showed that centrally administered angiotensin produced significant (p < 0.05) antidiuresis for 90 min. During this interval animals receiving angiotensin concentrated sodium and potassium in the urine (p < 0.01) and excreted equal or more absolute sodium and potassium than controls. During the interval from about 90–135 min, when the antidiuresis was over, angiotensin-treated rats excreted more urine of slightly greater sodium and potassium concentration than controls. Hence, angiotensin-treated rats had a significant deficit (p < 0.05) in absolute sodium and potassium when their urine volume became equal to control. During the 3rd h, all groups excreted similar volumes of urine. Both angiotensin groups recovered from the observed sodium loss during this time, but they still had a Significant deficit (p < 0.05) in absolute potassium at the termination of the experiment. These central effects of angiotensin (drinking, antidiuresis, sodium and potassium loss) suggest that the peptide may cause the central nervous system to perceive a state of hyperosmolality. The response of water ingestion and conservation with simultaneous sodium and potassium loss would then be expected homeostatic mechanisms. Possibly these effects may operate in the pathogenesis of certain clinical disorders of hypoosmolality, such as the syndrome of inappropriate ADH release.