1. To test the hypothesis that [Asp 1 ,Val 5 ]-angiotensin-(1–8)octapeptide ([Asp 1 ,Val 5 ]ANG II) is a more potent agonist to aldosterone secretion in the sodium-depleted animal than is [Asn 1 ,Val 5 ]angiotensin-(1–8)octapeptide ([Asn 1 ,Val 5 ]ANG II), local adrenal arterial infusion of the two peptides has been carried out in sheep with cervical adrenal autotransplants. 2. Neither [Asp 1 ,Val 5 ]ANG II nor [Asn 1 ,Vak 5 ]-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.

1. ACTH administration (20 μg day −1 kg −1 ) to sheep produces hypertension associated with a raised cardiac output and hypokalaemia. 2. The aim of the present experiments was to detail the haemodynamic changes associated with restoration of the extracellular potassium concentration in sheep with ACTH-induced hypertension. 3. After 7 days of ACTH treatment potassium chloride (10 mmol/h) was infused for 3 days to restore plasma [K + ] to the pre-ACTH value. 4. ACTH reduced plasma [K + ] from 4.4 ± 0.1 to 3.2 ± 0.2 mmol/l but 3 days of potassium chloride infusion returned plasma [K + ] to 4.3 ± 0.2 mmol/l. 5. ACTH increased mean arterial pressure from 67 ± 2 to 88 ± 1 mmHg in the first 7 days and it remained elevated during potassium chloride infusion (91 ± 5 mmHg on day 10). 6. Cardiac output rose with 7 days ACTH treatment from 4.9 ± 0.2 to 6.0 ± 0.6 l/min but fell progressively with potassium chloride infusion to 4.9 ± 0.3 l/min on day 10. 7. These studies suggest that potassium status or extracellular [K + ] may play a role in determining the haemodynamic profile associated with steroid-induced hypertension.

1. Administration of adrenocorticotropic hormone (ACTH) to sheep produced increases in mean arterial pressure within 24 h associated with an increase in cardiac output and cardiac rate. Both cardiac output and blood pressure remained elevated over the 5 days of ACTH treatment. 2. Administration of ACTH during β-adrenoreceptor blockade resulted in an increase in blood pressure without changes in cardiac output at 24 h. 3. Administration of a combined steroid infusion over 5 days produced increases in cardiac output identical with the effects of ACTH but with a substantially smaller effect on blood pressure. 4. These data suggest that the observed changes in cardiac output produced by ACTH treatment may be associated with high blood concentrations of adrenocortical steroids rather than being necessary for the development of the hypertension.

1. The angiotensin analogues Sar 1 -Ala 8 -angiotensin II (AII), Sar 1 -Ile 8 -AII, Sar 1 -Leu 8 -AII, Sar 1 -Thr 8 -AII, [Des 1 -Asp]-Ile 8 -AII and [Des 1 -Asp]-Sar 2 -Ile 8 -AII and converting enzyme inhibitor (SQ 80221) infused by intra-adrenal arterial infusion had no effect on aldosterone secretion in sodium-deficient sheep at doses in excess of those shown to block exogenous angiotensin II or III infusion. 2. It is suggested that the intrinsic agonist activity of the analogues may fulfil the requirements for a permissive role for angiotensin in the aldosterone response to sodium deficiency.

1. Acute severe sodium subtraction (20–25% of total exchangeable sodium) before or during treatment with adrenocorticotrophic hormone (ACTH) does little to modify the increase in blood pressure induced by ACTH. 2. Chronic low salt diet, less than 5 mmol/day, abolishes the blood pressure increase, but the response can be restored by increasing the sodium intake to as little as 10 mmol/day. 3. 17α,20α-Dihydroxyprogesterone infused concurrently with other adrenal steroids will mimic ACTH hypertension and perhaps represents a new class of steroid capable of influencing btood pressure.

1. The mechanism of adrenocorticotrophic hormone (ACTH)-induced hypertension in the sheep has been examined. 2. Hypertension was dependent on the presence of the adrenal gland. 3. ACTH-hypertension was not reproduced by administration of cortisol, corticosterone, deoxycorticosterone or deoxycortisol, alone or in combination. 4. Intact adrenal nerves were not necessary for the hypertension. 5. It is postulated that an adrenal factor other than those studied may be responsible for the hypertension.