Perspectives in aldosterone and renin control
Coghlan, J.P.; Blair-West, J.R.; Denton, D.A.; Scoggins, B.A.; Wright, R.D.
Australian and New Zealand Journal of Medicine 1(2): 178-197
1971
ISSN/ISBN: 0004-8291 PMID: 4327827 Document Number: 31196
The factors which control sodium excretion by the kidney - the glomerular filtration rate, the action of the steroid hormones to increase tubular reabsorption of sodium, and other influences on tubular reabsorption, often grouped together under the general heading of "third factor", e. g. proximal tubular salt losing hormone, oncotic pressure and vascular redistribution within the kidney - have been reviewed by Earley and Daugharty in 19691and Ehrlick in 19682. Aldosterone is the major mineralocorticoid of the adrenal gland and as such has an obvious ranking amongst those variables which can influence sodium metabolism. Aldosterone has another important relation with the kidney through the pressor peptide hormone angiotensin Ii which is one of the three factors known to be able to directly stimulate the zona glo-merulosa of the adrenal cortex to secrete aldosterone. Renin is a proteolytic enzyme released from the renal cortex which acts upon a specific globulin in plasma (renin substrate orangiotensino-gen) to produce the decapeptide angiotensin I. This in turn is converted into the hormone angiotensin Ii by the cleavage of a dipeptide from the C-terminal end. This conversion can be accomplished by "converting enzymes" which occur in blood or in the lungs. Angiotensin Ii is believed by some to be the most important variable in producing increased aldosterone secretion, especially during sodium restriction. Because this is believed to be the case, the factors which determine the angiotensin Ii level in blood could be more important than renin secretion per se, as this is only one sector of a complex system operating to increase arterial angiotensin Ii concentration.