From these studies, a number of conclusions can be drawn:(1) When high levels of circulating AII are present, iv saralasin acts as its antagonist: it produces a vasodepressor effect, decreases secretion of aldosterone and other steroids, and induces a number of hemodynamic changes, such as increased cardiac output and augmented blood flow in the most sensitive vascular beds, that is, the coronary and renal circulation. Therefore, it appears that in conditions of stimulated renin release, the above functions are under regulatory control by AII.(2) When circulating AII is suppressed, saralasin acts as an agonist analog: it produces a vasopressor action, stimulates steroidogenesis by the adrenals and causes changes in regional blood flow distribution by constricting or dilating regional vascular beds to different degrees, depending upon local receptor sensitivity.(3) The number and sensitivity of AII receptors and possibly their very nature differ from tissue to tissue and are affected greatly by the state of sodium balance. Thus, tissue reaction to AII or its derivatives may vary according to the molecular configuration of an octapeptide, the number of molecules present, or the abundance or scarcity of sodium ions.(4) There is definite evidence for the existence of specific AII receptors located in certain sites of the central nervous system. Direct excitation of these receptors produces effects on blood pressure, water intake, and release or metabolism of certain hormones. Most of these receptors, however, are" inside the blood-brain barrier" and apparently are inaccessible to circulating AII. Therefore, their importance in the regulation of the above activities remains obscure.