Effects of central and peripheral angiotensin blockade in hypertensive rats

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Abstract
The angiotensin II (AII) antagonist [Sar1-Ala8]AII (saralasin) was injected into the brain ventricles (IVT) and i.v. in 5 different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. I.v. infusions of cumulative doses (0.1-100 .mu.g/kg per min) and IVT injections (5-40 .mu.g) of saralasin did not change mean arterial pressure (MAP) in controls and in 1-clip, 1-kidney Goldblatt hypertension; MAP decreased in 1-clip, 2-kidney Goldblatt hypertension following i.v. and IVT saralasin. In 2-clip, 2-kidney hypertensive rats, IVT saralasin decreased MAP but was ineffective when infused i.v. Both i.v. and IVT saralasin increased MAP in DOC [deoxycorticosterone] hypertension. In spontaneously hypertensive (SH) rats, i.v. saralasin increased MAP; IVT injection decreased MAP. The effect of IVT saralasin in SH rats persisted 15-20 h after nephrectomy. Plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. Dissociation of the effects of i.v. and IVT saralasin and the persistence of blood pressure decrease in nephrectomized SH rats following IVT saralasin further support a role for locally formed brain angiotensin.