INTERRENAL FUNCTION IN LARVAL AMBYSTOMA-TIGRINUM .4. ACID-BASE-BALANCE AND THE RENIN-ANGIOTENSIN SYSTEM

Larval Ambystoma tigrinum were cannulated nonocclusively in the truncu s arteriosus and allowed to recover for 20-24 hr. In one group of anim als a peritoneal cannula was inserted in order to induce acidosis thro ugh the injection of lactic acid (2 mu mol/g). Immediately following a control blood sample (hr 0), lactic acid was injected, and blood samp les were collected at 1, 4, 8, and 24 hr and analzyed for pH, PCO2, PO 2, [HCO3-], and aldosterone. These animals exhibited a significant met abolic acidosis, which was accompanied by a significant increase in pl asma aldosterone, and recovered in approximately 24 hr. Additional gro ups of animals were subjected to the same acidosis and also received e ither saralasin (0.01 or 1 mu g/g at 0, 1, and 4 hr) or captopril (0.0 1-0.1 or 1 mu g/g at 0, 1, and 4 hr). The groups of animals whose reni n-angiotensin system was blocked by saralasin or captopril did not sho w a significant change in their ability to recover from the metabolic acidosis. Furthermore, saralasin and captopril were ineffective in inh ibiting the normal rise in circulating aldosterone in response to acid osis. In another group of animals, synthetic human angiotensin II (1 m u g/g; Ang II) was infused immediately following the control blood sam ple (hr 0) and blood samples were collected at 2, 4, 6, and 8 hr and a ssayed for aldosterone. Plasma aldosterone levels increased significan tly from 133 +/- 91 pg/ml at hr 0 to a maximum of 3288 +/- 519 pg/ml a t hr 4. Sham-treated animals did not increase circulating aldosterone. When Ang II (1 mu g/g) and saralasin (1 mu g/g) were given simultaneo usly, however, the rise in plasma aldosterone was only about 35% that of animals which received Ang II alone. We conclude that administratio n of Ang II leads, either directly or indirectly, to synthesis and rel ease of aldosterone from the interrenal tissues of larval Ambystoma ti grinum and that this rise can be significantly attenuated by saralasin . We furthermore conclude that although the renin-angiotensin system m ay be indirectly involved in recovery from an acid challenge, it does not appear to be the stimulus for the observed increase in plasma aldo sterone in response to acidosis in these animals. (C) 1997 Academic Pr ess