[Asp1, Val5] angiotensin-(1-8)octapeptide does not stimulate aldosterone secretion in sodium-depleted sheep.
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,Val5]-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.
D000450:Aldosterone / Q000378:metabolism*; D000802:Angiotensin Amide / Q000494:pharmacology; D000804:Angiotensin II / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D004039:Diet, Sodium-Restricted; D012756:Sheep; D012964:Sodium / Q000172:deficiency*; D013268:Stimulation, Chemical
D000804:Angiotensin II; D000450:Aldosterone; D000802:Angiotensin Amide; C031193:angiotensin II, Asp(1)-Val(5)-; D012964:Sodium