1. To test the hypothesis that [Asp1,Val5]-angiotensin-(1–8)octapeptide ([Asp1,Val5]ANG II) is a more potent agonist to aldosterone secretion in the sodium-depleted animal than is [Asn1,Val5]angiotensin-(1–8)octapeptide ([Asn1,Val5]ANG II), local adrenal arterial infusion of the two peptides has been carried out in sheep with cervical adrenal autotransplants.
2. Neither [Asp1,Val5]ANG II nor [Asn1,Vak5]-ANG II further stimulated the increased level of aldosterone secretion in conscious moderately sodium-depleted sheep. Greater sodium deficiency further increased aldosterone secretion.
3. The conclusion of Campbell, Schmitz & Itskovitz [Clinical Science (1979), 56, 325–333] that the free acid form of angiotensin II was a more potent agonist of aldosterone secretion than was the amide form under conditions of reduced sodium status is not supported by studies in sodium-depleted sheep.