Gee thanks. Here I am trying to avoid studying endocrine, and you post this. Anyway, I figured that must be the universe's way of telling me to get to it, so I looked you question up and here is what I found:
http://content.karger.com/ProdukteD...ikelNr=314315&Ausgabe=254530&ProduktNr=223855
Hypertension in CS is significantly correlated with the duration of hypercortisolism and results from the interplay between several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which are increased in this state. Glucocorticoids cause hypertension through several mechanisms: their intrinsic mineralocorticoid activity; through activation of the renin-angiotensin system; by enhancement of vasoactive substances, and by causing suppression of the vasodilatory systems. In addition, glucocorticoids may exert some hypertensive effects on cardiovascular regulation through the CNS via both glucocorticoid and mineralocorticoid receptors.
I also found this on Yahoo! Answers (not a great source, but it makes sense):
Aldosterone acts on its target tissues via the mineralocorticoid receptor. The problem is, this receptor is not specific for aldosterone. Cortisol can bind to it just as easily as aldosterone can. There is loads more cortisol in our bodies than aldosterone, so why doesn't the cortisol swamp the receptor and give us permanent hypertension?
The reason for this is that wherever you find the mineralocorticoid receptor, you also find an enzyme called 11-beta-hydroxysteroid dehydrogenase. This enzyme grabs the cortisol before it gets to the receptor, and converts it into cortisone, which doesn't bind to the receptor.
In Cushing's, there is too much cortisol and 11-beta-hydroxysteroid dehydrogenase is overwhelmed, so cortisol escapes and binds to the mineralocorticoid receptor and causes hypertension.
The main point I seem to get out of everything is that the HTN is caused by the mineralocorticoid effects of cortisol.
