Volume control and altered renal and adrenal responsiveness to angiotensin in essential hypertension: implications for treatment with converting enzyme inhibition.

Sodium intake has a substantial effect on target tissue responsiveness to angiotensin II (AII). These changes seem to be critical for normal regulation of sodium balance and blood pressure control. In a substantial number of patients with essential hypertension this normal sodium-mediated modulation of tissue responsiveness to AII is absent. These individuals may have either normal or high renin levels and can be characterized by a decreased adrenal responsiveness to AII on a low sodium intake and/or decreased vascular, particularly renal vascular, responsiveness to AII on a high sodium intake. While the underlying mechanisms are unclear, it is likely that a defect in the regulation of responsiveness to AII at the tissue level and/or its receptor is a major factor. The elevated blood pressure may result either from an alteration in renal sodium handling or inappropriate increases in AII levels, depending on ambient sodium intake. Thus, the patients can have either volume or AII-dependent hypertension. A most intriguing aspect of their disease process is that converting enzyme inhibitors appear to correct the underlying abnormality. If our hypothesis is confirmed, converting enzyme inhibitors may provide a more definitive and specific way to treat their hypertension than was anticipated when these drugs were developed.