Influence of sodium intake on vascular and adrenal angiotensin II receptors

The restriction of sodium intake reduces the sensitivity of vascular smooth muscle to angiotensin II, but enhances its influence on the adrenal glomerulosa cell. A competitive antagonist to angiotensin II, the Sar1, Ala8 derivative (P113), which shows affinity for the same receptor as angiotensin II, was used to examine the role of receptor affinity in the effect of sodium intake on these two systems in vitro. A threshold P113 concentration reduced the response to angiotensin of aortas derived from rabbits on a high, but not on a low, salt intake. Similarly, a threshold P113 concentration inhibited aldosterone response to angiotensin in glomerulosa cells obtained from sodium-loaded, but not sodium-restricted, rats. Large doses of P113 reduced the response to angiotensin in both preparations on either diet. The competitive antagonist presumably shares affinity for the same receptor on the basis of structural similarities; thus, the results suggest that sodium restriction blunts the vasoactive effects of angiotensin by reducing the affinity of its receptor for angiotensin. In contrast, the enhanced adrenal response to angiotensin with sodium restriction cannot be explained by an altered receptor-agonist interaction, but must reside in a change in an intracellular biochemical process, sufficient to overcome the influence of reduced receptor affinity.