Submitter: placido grino | placido_grino@yahoo.com
Published February 9, 2006
I've been curious for quite some time about the adaptive nature of renal vasoconstriction in the presence of volume expansion and increased distal delivery of Na, specially when it has been established that Na, and thus ECF balance hardly rely on the renal Na co-transport systems, as discussed in this editorial. By analogy, one must also question the adaptive nature of renal vasodilatation in the presence of decreased GFR and distal delivery of Na, presumably a marker of ECF volume depletion.
Perhaps TGF serves a much more imperious teleological purpose, that is, K homeostasis: if one contemplates how increased or decreased delivery of Na to the distal Na-K exchange segments of the nephron could convey the corresponding threats of hypo- and hyper-kalemia, respectively. Perhaps quality rather than quantity maintenance of body fluids is what's at work, at least within the span of physiologic conditions.
Such type of thinking about the TGF would help explain why Na intake beyond replacement needs (nowadays minimal in our modern sedentary and unsweating societies) constitutes such a threat for the development of hypertension. It would also be consistent with the manifest reluctance of the kidney to get rid of excessive dietary Na.