No abstract

The effect of electrolytic lesions of the subfornical organ on water intake induced by the continuous infusion of angiotensin-II through a chronic jugular cannula was studied. Lesions of the subfornical organ significantly reduced but did not abolish the elicited drinking. These results support the hypothesis that the subfornical organ is a receptor site for angiotensin-II but also suggest that this may not be the only site of receptors.

No abstract

The effect of the infusion of antiserum to angiotensin II on extracellular thirst was studied in rats. Drinking induced by the administration of polyethylene glycol or isoproterenol was reduced significantly when antiserum was infused. These results indicate that angiotensin is involved in drinking in response to extracellular dehydration.

Experiments were performed to investigate whether the copious drinking of rats infused with angiotensin II results from a reduction in plasma volume. Angiotensin II (Hypertensin, CIBA) dissolved in 0.9% NaCl was infused through a jugular cannula into conscious, unrestrained rats at a rate of 0.72 ± 0.015 μg kg−1 min−1 for a 30 min period. The amount of angiotensin II required to induce the first drinking response was 6.43 ± 0.667 μg/kg body weight and the latency to drink following the initiation of the infusion was 9.1 ± 0.97 min. The average intake of water during the first drinking bout was 6.3 ± 0.43 ml/kg. The total intake of water during the 30 min infusion period was 13.0 ± 1.37 ml/kg. Plasma volume and hematocrit were determined before and during the angiotensin II infusion. Blood samples were obtained from the jugular cannula before the infusion began and again either 1, 2, 3, 4, 5, 10, 15, or 30 min after the infusion began. The same determinations were also made either when angiotensin II initiated drinking, 2 min or 8 min thereafter. There were no significant changes in either plasma volume or hematocrit. It is concluded that angiotensin-induced drinking does not occur because of hypovolemia produced by angiotensin II.