Control of aldosterone secretion in domestic mammals during the perinatal period.

Aldosterone in ovine fetal circulation is mainly of fetal origin. Three of the renin-angiotensin system (RAS) parameters (renin, renin substrate and angiotensin II) originate in the fetus. The fetal RAS responds to stimulation (furosemide administration, hemorrhage, hypoxemia) or inhibition (phenylephrine or angiotensin II infusion) in a manner similar to that of the adult. The response of the fetal adrenal gland to angiotensin II is age-dependent and the near-term adrenal gland is not fully sensitive to angiotensin II and relatively insensitive to potassium (K+) as well as to adrenocorticotrophin hormone (ACTH) stimuli. In the newborn, the RAS is fully operative since it responds to diuretic stimulation in the lamb and the calf or to inhibition by angiotensin II administration in the lamb. Angiotensin II infusion, or angiotensin-converting enzyme blockade in the newborn lamb is followed by changes in plasma renin activity (PRA) or plasma aldosterone concentration (PAC) that suggest that angiotensin II regulates aldosterone secretion and that there is a negative feed back loop between angiotensin II and renin release. The newborn lamb adrenal gland is sensitive to potassium ions while in the newborn calf, ACTH stimulates cortisol secretion but fails to induce any change in PAC, suggesting that, in this species, the zona glomerulosa of the adrenal cortex is insensitive to ACTH.