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Spontaneous blood pressure recovery following hemorrhage in anesthetized rats is almost completely blocked by administration of captopril. This occurs despite comparable or enhanced increases in plasma levels of catecholamines and vasopressin. These findings suggest that angiotensin II, the formation of which is blocked by captopril, is essential to acute blood pressure recovery following hemorrhage and that changes in catecholamines or vasopressin are insufficient to sustain pressure recovery. The data also indicate that angiotensin II formation is not essential in the hemorrhagic stimulation of vasopressin or catecholamines.

By selective inbreeding of the Hebrew University Sabra rat, we have obtained a hypertension prone (H) and a hypertension resistant (N) substrain. The criteria for selection was the blood pressure response to DOCA-salt. The outstanding element of our model is the N rat with its remarkable resistance to hypertension. When compared to H, the N rat presents the following characteristics: 1. The blood pressure of experimentally naive N rats is significantly lower at comparable ages, in both sexes. 2. N rats are resistant to both DOCA-salt and renal clip hypertension. 3. In the medulla oblongata (MO) of N rats, the noradrenaline (NA) content is significantly higher and the activity of tyrosine hydroxylase is significantly lower. 4. In the MO of N rats, the sensitivity of the NA dependent cAMP generating system is significantly decreased. 5. In the atrium of N rats, the NA content is significantly higher, and is unaffected by DOCA-salt treatment. The results suggest that genetic differences in catecholamine metabolism may account for the disparate susceptibility to hypertension of the two strains.