Excess Catecholamine Syndrome and the renin angiotensin aldosterone system

Excess Catecholamine Syndrome and the renin-angiotensine II-aldosterone system
Since the early days of hypertension research it is well accepted that a malignant hypertension as a consequence of kidney injury leads to a pronounced secretion of renin with the consecutive formation of angiotensin II and aldosterone. Even under these conditions, a beta-blockade reduces renin secretion and blood pressure. Furthermore, renin secretion is strongly reduced after an anesthesia-induced inhibition of sympathetic influences although the kidney perfusion is diminished (1). A healthy kidney is expected to release only small amounts of renin. An increased sympathetic outflow of the brain induces, however, a deleterious rise in renin release. Angiotensin II promotes not only norepinephrine release from sympathetic nerve endings but stimulates autonomic centers in the brain that enhance sympathetic efferences. In addition, angiotensin II stimulates the production of aldosterone which causes sodium retention. It can thus be concluded that several re-enforcing mechanisms exist which promote manifestation of hypertension.

1. Zayas VM, Blumenfeld JD, Bading B, McDonald M, James GD, Lin YF, Sharrock NE, Sealey JE, Laragh JH: Adrenergic regulation of renin secretion and renal hemodynamics during deliberate hypotension in humans. Am J Physiol 1993;265:F686-92