There is emerging evidence that
cortisol plays a significantly greater role in human
hypertension than previously thought. Apart from the well recognized role of
cortisol in the
hypertension of
Cushing's syndrome, local
cortisol excess has been recognized as responsible for rare forms of
hypertension such as apparent
mineralocorticoid excess and licorice abuse and more recently implicated in the
hypertension of
chronic renal failure,
hypertension related to low birth weight and
essential hypertension. Although
cortisol-induced
hypertension is characterized by
sodium retention and volume expansion, studies with synthetic
glucocorticoids or
sodium restriction suggest that the
hypertension is, to a substantial degree, independent of
sodium and volume. Increase in cardiac output is not essential for
cortisol-induced blood pressure rise but the precise role of increases in total or regional peripheral resistance as a primary mechanism has nto been determined. Increased pressor responsiveness, particularly to
catechols, is a prominent feature but whether these changes are sufficient to account for the
hypertension remains unclear. There is no evidence for increased sympathetic nervous activity as judged by measurements of plasma catcholamines,
neuropeptide-Y, or resting
noradrenaline spillover rate. Responses to mental stress or maximal hand-grip are unchanged and baroreflex sensitivity is increased.
Octreotide profoundly reduced the elevated plasma
insulin concentrations seen with
cortisol administration but had no effect on the rise in blood pressure.