Role of angiotensin II in aldosterone regulation in the Pekin duck.
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 membrane-binding techniques, suggesting that the AII effect on aldosterone secretion is direct. Angiotensin II produced no change in plasma corticosterone. The infusion of KCl 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.
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Max-Planck-Institut für Physiologische und Klinische Forschung, W. G. Kerckhoff-Institut, Bad Nauheim, Federal Republic of Germany.
Gerstberger
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Simon
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D000311:Adrenal Glands / Q000032:analysis; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000805:Angiotensin III / Q000494:pharmacology; D000818:Animals; D004372:Ducks / Q000378:metabolism*; D005260:Female; D008297:Male; D011189:Potassium Chloride / Q000494:pharmacology; D011945:Receptors, Angiotensin / Q000032:analysis; D012964:Sodium / Q000097:blood
D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000805:Angiotensin III; D000450:Aldosterone; D011189:Potassium Chloride; D012964:Sodium