Interrenal function in larval Ambystoma tigrinum. IV. Acid-base balance and the renin-angiotensin system.
Larval Ambystoma tigrinum were cannulated nonocclusively in the truncus arteriosus and allowed to recover for 20-24 hr. In one group of animals a peritoneal cannula was inserted in order to induce acidosis through the injection of lactic acid (2 micromol/g). Immediately following a control blood sample (hr 0), lactic acid was injected, and blood samples were collected at 1, 4, 8, and 24 hr and analyzed for pH, PCO2, PO2, [HCO3-], and aldosterone. These animals exhibited a significant metabolic acidosis, which was accompanied by a significant increase in plasma aldosterone, and recovered in approximately 24 hr. Additional groups of animals were subjected to the same acidosis and also received either saralasin (0.01 or 1 microg/g at 0, 1, and 4 hr) or captopril (0.01-0.1 or 1 microg/g at 0, 1, and 4 hr). The groups of animals whose renin-angiotensin system was blocked by saralasin or captopril did not show a significant change in their ability to recover from the metabolic acidosis. Furthermore, saralasin and captopril were ineffective in inhibiting the normal rise in circulating aldosterone in response to acidosis. In another group of animals, synthetic human angiotensin II (1 microg/g; Ang II) was infused immediately following the control blood sample (hr 0) and blood samples were collected at 2, 4, 6, and 8 hr and assayed for aldosterone. Plasma aldosterone levels increased significantly from 133 +/- 91 pg/ml at hr 0 to a maximum of 3288 +/- 519 pg/ml at hr 4. Sham-treated animals did not increase circulating aldosterone. When Ang II (1 microg/g) and saralasin (1 microg/g) were given simultaneously, however, the rise in plasma aldosterone was only about 35% that of animals which received Ang II alone. We conclude that administration of Ang II leads, either directly or indirectly, to synthesis and release of aldosterone from the interrenal tissues of larval Ambystoma tigrinum and that this rise can be significantly attenuated by saralasin. We furthermore conclude that although the renin-angiotensin system may be indirectly involved in recovery from an acid challenge, it does not appear to be the stimulus for the observed increase in plasma aldosterone in response to acidosis in these animals.
Eskandari
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Biological Sciences Department, California State Polytechnic University, Pomona, California, 91768, USA. sepehr@physiology.medsch.ucla.edu
Stiffler
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D000136:Acid-Base Equilibrium / Q000187:drug effects / Q000502:physiology*; D000138:Acidosis / Q000097:blood / Q000139:chemically induced / Q000378:metabolism / Q000662:veterinary; D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D000557:Ambystoma / Q000196:embryology / Q000502:physiology*; D000804:Angiotensin II / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001784:Blood Gas Analysis; D002216:Captopril / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D007401:Interrenal Gland / Q000187:drug effects / Q000502:physiology*; D008297:Male; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D012504:Saralasin / Q000494:pharmacology; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D000450:Aldosterone; D002216:Captopril; D012504:Saralasin