Restoration of suppressed baroreflex sensitivity in rats with hereditary diabetes insipidus (Brattleboro rats) by arginine-vasopressin and DDAVP.

To determine the influence of vasopressin on baroreceptor reflex mechanisms, baroreflex function in Brattleboro rats was compared with that in normal Long-Evans rats. Baroreflex function was assessed in conscious unrestrained rats during increases in blood pressure with phenylephrine (200 Mg/kg per min for 10 seconds). The baroreflex function line was obtained by plotting the log (pulse period) against the preceding systolic pressure on a beat-by-beat basis. The slope of the baroreflex function line (baroreflex function slope) in Long-Evans rats [(19.0 ± 1.4) X 10", mean ± SEM, n = 34] was significantly steeper than that in Brattleboro rats [(6.9 ± 0.6) X 10~\ n = 44, P < 0.001]. A subpressor intravenous infusion of arginine-vasopressin (2 ng/kg per min for 2 hours), which elevated plasma vasopressin to 48.1 ± 6.8 pg/ml, caused bradycardia and increased the baroreflex function slope in Brattleboro rats, from (7.5 ± 1.0) x 10"" to within the normal Long-Evans range [(17.0 ± 0.8) x 10~\ n = 7, P < 0.001]. The basal pulse period and the baroreflex function slope in Brattleboro rats [(7.0 ± 0.9) x 10~] was also increased significantly to (12.0 ± 1.7) X 10"* (n = 11, P < 0.01) by an infusion of l-desamino-8D-arginine vasopressin, (2 ng/kg per min for 2 hours), a vasopressin analogue with potent antidiuretic but minimal vascular actions. Acute volume expansion, which increased body weight significantly, did not change the baroreflex function slope in Brattleboro rats [(7.7 ± 1.1) X 10" vs. (8.2 ± 1.7) X 10~\ n = 6]. A specific vasopressin vascular receptor antagonist [d(CH2)5 Tyr(Me)AVP], although blocking the pressor effect of exogenous vasopressin, did not change the pulse period or the baroreflex function slope [(16.0 ± 2.3) X 10~* vs. (19.0 ± 1.7) X 10"*, n = 6)] in normal Long-Evans rats. The results obtained in Brattleboro rats and the change in baroreflex sensitivity brought about by infusions of vasopressin and DDAVP provide strong evidence that vasopressin may be an important physiological modulator of baroreflex function. (Circ Res 53: 140-149, 1983)