Saralasin was administered to 9 normotensive volunteers and 13 patients with essential hypertension after sodium depletion and sodium repletion. 2) In standing normotensive volunteers, angiotensin II inhibition induced significant hypotension if previously a cumulative sodium loss of at least 160-200 mEq had been induced. 3) In patients with essential hypertension, saralasin infusion induced either blood pressure reduction, no change or even significant blood pressure increase, depending on the prevailing state of sodium balance. 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. 5) Saralasin administration to patients with essential hypertension may not only be useful for recognizing renin dependency but may also, via the slight intrinsic agonistic effect of the compound, permit identification of overactivity of the sodium factor.
