Hyponatremia developing some days after transsphenoidal pituitary adenectomy is a treacherous complication of uncertain cause. Of 19 patients monitored in a pilot study at the Wessex Neurological Centre, plasma sodium fell below 125 mmol/liter in three patients at times ranging from 6 to 9 days postoperatively. One patient had evidence of inappropriate secretion of arginine vasopressin (AVP), and the other two probably had steroid insufficiency despite apparently adequate steroid cover. In a more detailed study, the fluid and sodium balance of a further 16 patients was monitored for 7 to 11 days following transsphenoidal surgery together with plasma cortisol, renin, and AVP concentrations. No patient became severely hyponatremic. Three developed partial diabetes insipidus. Two patients with Cushing's disease had evidence of postoperative corticosteroid insufficiency despite normal steroid protection. An inappropriately low plasma cortisol concentration was recorded in both. Plasma AVP concentrations did not show a delayed surge postoperatively. Delayed hyponatremia appears to occur most often in patients with hypoadrenalism, as glucocorticoid cover is decreased. It results from water retention combined with natriuresis, and is reversed by glucocorticoid treatment.

SUMMARY1. Active and acid-activatable (inactive) renins were measured in rabbit plasma under control conditions and during sodium depletion with subsequent repletion.2. Active renin increased by 97 % during sodium depletion and returned to control levels on repletion. Both, changes were complete within 1 day of changing the diet.3. During dietary sodium depletion inactive renin levels initially fell to zero and then increased until, after 13 days, inactive renin was again 10% of total renin levels, a proportion comparable to the control values.4. Sodium repletion caused plasma inactive renin to return to control levels over about 13 days, a quite different time course to active renin. Therefore, in the first phase of repletion the proportion of total renin in the inactive form rose to 19 %.5. These changes are discussed in relation to concurrent changes in sodium, potassium and water metabolism.

1. Renin activity in rabbit plasma increases after acidification (pH 3.3), probably due to activation of an inactive form of renin. 2. Both active and inactive renin in plasma increase after haemorrhage. This stimulus does not change the relative proportions of the two forms. 3. After ligation of the renal blood vessels neither form of renin increases in response to haemorrhage. 4. One day after bilateral nephrectomy no inactive renin could be demonstrated in plasma. 5. In the rabbit, therefore, the kidney is a major source of the inactive renin in plasma.

SUMMARY1. Active and inactive renin release by rabbit kidney cortex slices was investigated. Inactive renin was estimated as the increase in renin activity after acidification (pH 2 8) of slice supernatant solutions.2. Active renin release was increased when incubation medium [Na+] was reduced. This relationship was linear (r2 = 0 96) over the range [Na+] = 23-133 mM.3. For the same range of [Na+] inactive renin secretion decreased when medium [Na+] was reduced (r2 = 0 92). Therefore, the proportion of total renin which was in the inactive form decreased linearly as [Na+] was reduced (r2 = 0-97).4. Chloride ions did not appear to be important in altering the secretion of either active or inactive renin.5. Adding furosemide to the incubation medium in concentrations up to 40 ,ug/ml.did not change secretion of either form of renin. The action of furosemide on secretion of active and inactive renin in vivo is therefore secondary to altered renal function.6. Regulation of the relative amount of active and inactive renin in plasma could be entirely an intrarenal event. It is not essential to invoke a plasma activating enzyme for inactive renin in order to explain changes in plasma levels of the two forms of renin.7. This paper supports the hypothesis that release of inactive renin by the kidney is controlled by a sodium-sensitive mechanism.

SUMMARY1. Release of active and inactive renin by rabbit kidney cortex slices was investigated. Inactive renin was estimated as the increase in renin activity after acidification (pH 2 8) of slice supernatant solutions.2. In Ca2+-free media, release of both active and inactive renin was increased but the changes in inactive renin were more marked. The percentage of total renin released which was inactive ranged from 8'3 % ([Ca2+] = 9-2 mM) to 34-5 % (zero 6. Mechanisms controlling the secretion of active and inactive renins by the kidney are at least partially independent. Differential secretion of the two forms, perhaps linked to regulation of the activation of inactive renin before release, appears to be the basis of a control step in the over-all expression of the renin-angiotensin system. This may be coupled in some way to juxtaglomerular cell Na+ ion flux.