ABSTRACT
Everyone interested in the pathogenesis of essential hypertension believes that this does not represent a single process with a single pathogenesis. Indeed, over the past century and a half, advances in our understanding have had a characteristic sequence: a specific mechanism was identified in a subset of patients, which became a form of ‘secondary hypertension’. Chronic renal failure recognized by Bright early in the nineteenth century remains the most common secondary cause. The last hundred years have seen the identification of Cushings syndrome, pheochromocytoma, primary aldosteronism, coarctation of the aorta, renovascular hypertension, and several monogenic forms of hypertension, e.g. glucocorticoid remedial hypertension (GRA), apparent mineralocorticoid excess syndrome, and Liddle’s syndrome. Thus, essentially all of the identifiable causes to date are dominated by the kidney and the adrenal. Moreover, the logic has involved removing from a large group of patients with a similar phenotype – elevated blood pressure – subgroups of patients with an identifiable pathogenesis. It is appropo of nonmodulation that the first indication of an important renal and adrenal contribution was made by Bright and Addison in the same institution, Guys Hospital. This chapter will focus on one substantial subgroup involving perhaps 40% of patients with normal and high renin essential hypertension who show an abnormality involving the control of the kidney and the adrenal aldosterone release in response to shifts in sodium intake.1 Again, a single institution was involved.
