The role of endogenous vasopressin in cardiovascular homeostasis was examined using vasopressin-deftcient rats (Brattleboro) (n=194) and their parent strain, Long-Evans rats (n=181). Mean arterial pressure (blood pressure) and heart rate were measured every 4 seconds with or without infusion of drug solution for 21 hours, and mean values and their standard deviations (lability) were calculated. Blood pressure in Brattleboro rats (116±1.1 mm Hg, mean±SEM) was significantly higher than that in Long-Evans rats (96±0.7 mm Hg, /><0.001), whereas heart rates (381±33 and 375±2.9 beats/min, respectively) were similar. The lability of blood pressure and heart rate in Brattleboro rats (9.2±0.1 mm Hg and 42 J±0.7 beats/min) was also greater than that in Long-Evans rats (6.7 ±0.1 mm Hg, p< 0.001 and 38.4±0.8 beats/min, p<0.0l, respectively). In Brattleboro rats, intravenous vasopressin (0.1 ng/kg/min or 0.6 ng/kg/min) did not affect blood pressure, although it did reduce heart rate and decreased lability of blood pressure and heart rate. Intracerebroventricular (central) infusion of vasopressin (2 pg/kg/min) in Brattleboro rats induced initial hypertension and tachycardia followed by long-lasting hypotension and bradycardia, whereas in Long-Evans rats it induced only hypertension and tachycardia. In both strains, central vasopressin dramatically decreased the lability of blood pressure and heart rate. A rginine vasopressin (AVP) has long been known to possess potent vasoconstrictor properties. 1 However, when AVP is infused intravenously into conscious animals or humans, there is no increase in blood pressure until extremely high plasma AVP levels are achieved. 2 Evidence has accumulated indicating that the absence of increases in blood pressure in response to AVP infusion in normotensive animals may be due to the presence of an effective and specific buffering system. 3 -5 On the basis of available evidence, it has been proposed that the locus of this buffering system is in the central nervous system. 6 -12 Recently, it has been reported that Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI rats) have suppressed baroreceptor reflex sensitivity. 9 Exogenous AVP and the V 2 renal receptor agonist desmopressin (DDAVP) administered systemically is able to restore this suppressed sensitivity to within the range that is normal for Long-Evans (LE) rats. 9 It is believed that the inhibition of baroreceptor reflex pathway raises blood pressure. 13 Therefore, it may be postulated that rats with suppressed baroreceptor reflex mechanisms will have higher blood pressure and heart rate and a greater lability of blood pressure and heart rate than normal rats. Furthermore, we previously reported that centrally administered AVP lowered blood pressure in DI rats as well as in stroke-prone by guest on May 11, 2018 http://hyper.ahajournals.org/ Downloaded from