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Comparisons of aldosterone responses to [des-Asp1]-angiotensin II and angiotensin II, often at single dose levels, have shown a wide range of potency ratios. Therefore four-point dose–response comparisons were performed in sodium-replete sheep, using i.v. infusion rates of angiotension II and angiotensin II amide that reproduced the physiological range of blood concentration of angiotensin II for sheep. Angiotensin III was infused i.v. at the same rates. Effects on arterial blood pressure, cortisol secretion rate, adrenal blood flow and plasma levels of Na+ and K+ were also compared. The potency ratio, angiotensin III: angiotensin II amide, was 0·87 for actual aldosterone secretion rate and 0·90 for the calculated increase in aldosterone secretion. For angiotensin III: angiotensin II the ratios were 0·80 and 0·91 respectively. These ratios were not significantly different from 1·00 but the tendency for angiotensin II to be slightly more potent was probably due to a contribution from derived angiotensin III during infusion of angiotensin II. Angiotensin II or angiotensin II amide was ∼ four times as potent as angiotensin III in raising arterial blood pressure. Cortisol secretion rate was slightly but significantly increased by all peptides at the higher infusion rates. Infusions had no effect on adrenal blood flow or plasma levels of Na + but raised plasma levels of K + slightly. These results confirm the conclusion from adrenal arterial infusion experiments that angiotensin II and III are almost equipotent in stimulating aldosterone secretion in sheep.
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Metoclopramide (10 mg i.v. injection followed by 10 mg/h i.v. for 2 h) caused a transient rise in blood concentrations of aldosterone in sodium-replete and sodium-depleted sheep. Infusion of metoclopramide into the adrenal artery of sheep with an autotransplanted adrenal gland, at a rate to give a similar concentration of metoclopramide at the adrenal cell level (calculated from rate of infusion and adrenal blood flow), resulted in no alteration in aldosterone secretion rate in either sodium-replete or sodium-depleted animals, even though intravenous metoclopramide caused transient stimulation of aldosterone secretion in the same sheep when sodium replete.
Dopamine administered either into the adrenal arterial blood supply or intravenously had no significant effect on aldosterone secretion and did not reverse the stimulatory effects of angiotensin II on aldosterone secretion in the adrenal transplant.
The data do not support the suggestion that direct dopaminergic elements play a tonic inhibitory role in aldosterone secretion. It is possible that the agonist effect of metoclopramide on aldosterone secretion may occur by some non-dopaminergic mechanism and it is tempting to speculate that the effect is centrally mediated.
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SUMMARY
Peripheral blood corticosteroid levels were determined in nine species of Australian marsupial (Eastern grey kangaroo, black-tailed, Bennett's and pademelon wallabies, quokka, wombat, koala and Western native and tiger cats), one species of monotreme (echidna) and one placental Australian mammal (dingo). Animals were obtained or bled with minimal disturbance and came from areas considered to have adequate sodium content of the vegetation. Aldosterone, corticosterone, cortisol, 11-deoxycorticosterone and 11-deoxycortisol were measured and levels found to be similar to five introduced eutherian species (sheep, cow, dog, fox and man) with the exception of the koala and the wombat. Cortisol was the predominant corticosteroid, except in the koala, which produced corticosterone in relatively the greatest quantity, and the wombat which produced more 11-deoxycortisol. Steroid levels were generally low in the wombat. ACTH administered to the koala changed its pattern of corticosteroid secretion from predominantly corticosterone to cortisol. In the dingo, administration of ACTH caused rises in corticosteroid levels similar to those seen in most other eutherian mammals.
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ABSTRACT
9α-Fluorocortisol has been postulated to have 'hypertensinogenic' as well as 'mineralocorticoid' and 'glucocorticoid' activity. The present study examined the blood pressure and metabolic effect in sheep of the structurally related steroids 9α-fluorodeoxycorticosterone (9α-FDOC) and 9α-fluorocorticosterone (9α-FB). Infusions of these fluorinated steroids at 0·63 and 0·67 mg/day respectively for 5 days produced falls in plasma potassium, but only 9α-FB increased urine volume. 9α-FDOC raised mean arterial pressure by 11 mmHg and 9α-FB raised it by 14 mmHg. Addition of a 9α-fluoro group appears to increase both 'mineralocorticoid' and 'hypertensinogenic' steroid potencies.
J. Endocr. (1985) 104, 291–294
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Plasma renin activity (PRA) and blood aldosterone and deoxycorticosterone levels were measured in Australian lungfish. Plasma renin activity was depressed after intravenous infusions of iso-osmotic (0·6%) NaCl but not after hypo-osmotic (0·3%) infusions. The presence of PRA in this fish is consistent with prior reports of renal renin activity in other sarcopterygian fishes. The results of the infusion experiments suggest that a fall in plasma osmolality or electrolyte concentrations may oppose the reduction in renin release in response to volume expansion.
Aldosterone and deoxycorticosterone were identified in the blood of Neoceratodus. The concentrations of both appeared higher in females than in males. Infusions of [5-valine]-angiotensin II amide for 2–4 h at rates known to increase blood pressure in this species did not alter blood aldosterone concentrations. This negative finding may suggest that the renin/angiotensin system is not involved in aldosterone regulation in Neoceratodus or that angiotensin receptors involved in regulation of steroidogenesis have a greater specificity for endogenous angiotensin than do vascular receptors.
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SUMMARY
The effect of sodium depletion on the conversion of corticosterone to aldosterone has been examined in vivo using the adrenal transplants of two sheep. [3H]Corticosterone was infused continuously directly into the adrenal gland via the carotid artery over a period of 30 min. and the total adrenal effluent was collected via the jugular vein in six consecutive 5-min. samples. The conversion of [3H]corticosterone to [3H]aldosterone and the endogenous output of aldosterone was measured in each sample using a double isotope derivative method and the specific activity of the aldosterone calculated. Radioactive conversion of B → aldosterone reached equilibrium within 10 min. of the start of infusion and remained constant over a period of 10–25 min. Aldosterone secretion was also constant during the first 25 min. of infusion.
In the same sheep the mean percentage conversion increased as aldosterone secretion rose over a range of 2–12 μg./hr. With more severe sodium depletion, i.e. with aldosterone secretion rates of 12–16 μg./hr., conversion decreased to that found in the sodium replete state. The specific activity of the aldosterone was constant throughout the mildly deplete range (2–12 μg./hr.) but fell with severe sodium depletion. In the sodium replete range (0–2 μg./hr.) before the introduction of a parotid fistula, the specific activity was the same as in the mildly deplete state. After the introduction of a parotid fistula the specific activity increased as the secretion decreased from 2 to 0 μg.
The validity of the approach and interpretation of the results in terms of the biosynthetic pathways involved are discussed.
