THE DIRECT EFFECT OF INCREASED SODIUM CONCENTRATION IN ADRENAL ARTERIAL BLOOD ON CORTICOSTEROID SECRETION IN SODIUM DEFICIENT SHEEP

Abstract

Summary Sheep with autotransplanted adrenal glands were made sodium deficient by continuous uncompensated loss of saliva from a parotid fistula for 2–3 days. The mean decrease of plasma sodium concentration was 9 mEq./l. Adrenal arterial infusion which increased the sodium concentration in the Mood supply of the transplanted adrenal gland by 5–30 mEq./l. did not stop the aldosterone hypersecretion caused by established sodium deficiency. Thus, local decrease of sodium concentration was not the sole or a major cause of aldosterone secretion in sodium deficiency. However, in sodium deficiency a mean increase in adrenal blood sodium concentration of 8 mEq./l. caused an approximately 25% decrease of aldosterone secretion rate during 1–3 hr. This significant suppression of aldosterone secretion rate tended to disappear over 3–6 hr. despite continued infusion or increase of adrenal arterial infusion rate, so that mean increase of adrenal plasma sodium concentration was 15 mEq./l. Infusions of hypertonic mannitol solution causing similar increase of osmotic pressure of adrenal plasma did not cause similar reduction of aldosterone secretion. In experiments made at the onset of sodium deficiency, aldosterone secretion rate continued to increase despite adrenal arterial infusion of NaCl which increased adrenal plasma sodium concentration by 2–4 mEq./l. This adrenal plasma sodium infusion was adequate to correct any fall of local sodium concentration occurring as a result of onset of sodium deficiency. Increase of adrenal plasma sodium concentration by 6–15 mEq./l. at the onset of sodium deficiency usually caused a large decrease of aldosterone secretion which was sustained. In some instances secretion rate returned to the sodium replete range. After stopping the adrenal arterial infusion aldosterone secretion rose rapidly. The results were consistent with an hypothesis that increase of sodium concentration in adrenal arterial blood in established sodium deficiency deleted the effect of that minor component of the hypersecretion of aldosterone caused by reduction of systemic plasma sodium concentration. An alternative interpretation is that the increased plasma sodium concentration to some extent antagonized the effect of the non‐ionic humoral stimulus of aldosterone secretion. The results indicated also that at the onset of sodium deficiency the mechanisms of stimulation of the adrenal were more sensitive to increase of plasma sodium concentration than in established sodium deficiency.