SUMMARY The contribution of vasopressin and angiotensin II to the maintenance of blood pressure after short-term autonomic blockade was investigated in conscious Long-Evans and Brattleboro (vasoprcssin-deficient; hereditary diabetes insipidus) rats. After short-term autonomic blockade by atropine (1 mg/kg), propranolol (5 mg/kg), and pentolinium (5 mg/kg and 10 mg/kg/hr), the fall in blood pressure was significantly greater in Brattleboro rats than in Long-Evans rats (48 ± 3 vs 32 ± 2 mm Hg; p < 0.01). Administration of the vasopressin vascular receptor antagonist D(CH 2 ) 5 Tyr-(Me)AVP (2 /^g/kg) caused further blood pressure decreases only in Long-Evans rats, so that the final blood pressure in both groups was identical. Administration of enalaprilat (10 mg/kg), an angiotensin converting enzyme inhibitor, further reduced blood pressure in both strains. When enalaprilat was given first after autonomic blockade, it reduced blood pressure in Brattleboro rats but not in LongEvans rats. Administration of the vasopressin antagonist after enalaprilat further reduced blood pressure only in Long-Evans rats. The fall in blood pressure following vasopressin blockade was greater than that occurring after angiotensin converting enzyme inhibition (14 ± 1 vs 6 ± 1 mm Hg; p < 0.05) in autonomic blockaded Long-Evans rats. Plasma levels of vasopressin in Long-Evans rats increased markedly after short-term autonomic blockade, whereas plasma renin and angiotensin II levels were unchanged. Plasma angiotensin II levels were increased by the vasopressin antagonist and decreased by enalaprilat. We conclude that, due to sympathetic nervous system blockade and consequent blunting of renal renin release, vasopressin has a greater capacity than the renin-angiotensin system for maintaining blood pressure after short-term autonomic blockade. (Hypertension 7: 547-553, 1985) KEY WORDS • renin • Brattleboro rat • hypertension • hypotension • converting enzyme inhibition * vascular tone B LOOD pressure (BP) regulation is a multifactorial phenomenon involving numerous complex interactions.1 " 3 The three major pressor mechanisms influencing BP are the autonomic nervous system and the vasoactive peptides angiotensin and vasopressin. The importance of the autonomic nervous system in cardiovascular control mechanisms is well defined, and the role of the renin-angiotensin system in various physiological and hypertensive or hypotensive