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The response of plasma aldosterone to increased plasma angiotensin II (AII) was evaluated in normally hydrated Pekin ducks as well as in birds in which plasma sodium had been acutely increased (+12 mmol/l) or reduced (–4 mmol/l) by the prior infusion of hypertonic saline or hypotonic glucose. In all cases, the i.v. infusion of AII at rates of 5, 15 and 45 pmol/kg per min for 1 h produced dose-dependent increases in the plasma concentration of aldosterone, with a potency that was inversely related to the sodium status. In addition, adrenal receptors for AII were demonstrated by in-vitro autoradiography and membranebinding techniques, suggesting that the AII effect on aldosterone secretion is direct. Angiotensin II produced no change in plasma corticosterone.

The infusion of KC1 at 1, 2 and 5 mmol/l for 1 h increased plasma potassium by as much as 2 mmol/l, but had no influence on plasma aldosterone. Similarly, the heptapeptide angiotensin III, infused at 5, 15 and 45 pmol/kg per min for 1 h had no effect on circulating aldosterone.

The results show that in ducks, AII has a physiological role in the control of aldosterone, whereas plasma potassium and angiotensin III have no such secretagogue function.

Journal of Endocrinology (1989) 123, 445–452

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