1. Angiotensin may influence arterial pressure either by direct vasoconstriction or by more slowly developing effects on thirst and renal function. The importance of direct vasoconstriction was estimated in rats during salt deprivation and renal hypertension by observing the fall in blood pressure that immediately followed injection of converting-enzyme inhibitor.
2. Chronically salt-deprived rats had normal arterial pressure, cardiac output and total peripheral resistance before inhibition. However, inhibiting the formation of angiotensin II caused marked decreases in arterial pressure (−47 mmHg) and total peripheral resistance (−30%).
3. Animals made hypertensive by renal artery constriction showed large decreases in arterial pressure when angiotensin formation was inhibited only during the first few days after constriction. In the chronic, benign phase of hypertension, animals with both clamp plus contralateral nephrectomy and with unilateral clamp only, showed decreases in pressure after inhibition (−12 to 16 mmHg) that were only slightly greater than decreases observed in normotensive control animals.
4. These results indicate that total peripheral resistance and the activity of the renin-angiotensin system can change separately. In salt deprivation, even though an increased fraction of resistance was due to angiotensin, total peripheral resistance was normal. In chronic renal hypertension, total resistance was undoubtedly elevated, but only partially because of the vasoconstrictor effect of angiotensin.