Escape from the sodium-retaining effects of mineralocorticoids

In our opinion, it is unlikely that a single factor mediates escape. Interruption of a single system, as repeatedly demonstrated in this review, does not prevent escape, probably due to activation of other mechanisms. For this reason, the evidence does not firmly rule out the participation of many of the individual mechanisms discussed in this review. Most likely, an interplay of several compensatory mechanisms mediates escape from the salt-retaining effect of mineralocorticoids. As stated by Smith, 'where multiple controls are super-imposed on a function, such as sodium excretion, it is conceived that normal regulatory mechanisms may be obscured by compensatory reactions'. The mechanism for escape from the salt-retaining effects of mineralocorticoids is not proven. In consideration of all of the foregoing, our current view of the mechanism for escape is as follows: Salt and water retention leads to expansion of an effective vascular volume, stimulation of volume receptors, and subsequent decreases in renal adrenergic activity. This decreased renal adrenergic activity directly decreases sodium transport as well as vasodilates the kidney, allowing increased transmission of systemic blood pressure to the renal vasculature. These factors, perhaps modulated by intrarenal hormones, increase sodium excretion and thereby mediate the escape from the salt-retaining effects of mineralocorticoids.