Vasopressin V-2 receptor enhances gain of baroreflex in conscious spontaneously hypertensive rats

The aim of the present study was to determine the receptor subtype involved in arginine vasopressin (AVP)-induced modulation of baroreflex function in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats using no vel nonpeptide AVP V-1- and V-2-receptor antagonists. Baroreceptor heart ra te (HR) reflex was investigated in both SHR and WKY rats which were intrave nously administered the selective V-1- and V-2-receptor antagonists OPC-212 68 and OPC-31260, respectively. Baroreflex function was assessed by obtaini ng alternate presser and depressor responses to phenylephrine and sodium ni troprusside, respectively, to construct baroreflex curves. In both SHR and WKY rats baroreflex activity was tested before and after intravenous admini stration of vehicle (20% DMSO), OPC-21268 (10 mg/kg), and OPC-31260 (1 and 10 mg/kg). Vehicle did not significantly alter basal mean arterial pressure (MAP) and HR values or baroreflex function in SHR or WKY rats. The V-1-rec eptor antagonist had no significant effect on resting MAP or HR values or o n baroreflex parameters in both groups of rats, although this dose was show n to significantly inhibit the presser response to AVP (5 ng iv; ANOVA, P < 0.05). In SHR but not WKY rats the V-2-receptor antagonist significantly a ttenuated the gain (or slope) of the baroreflex curve (to 73 +/- 3 and 79 /- 7% of control for 1 and 10 mg/kg, respectively), although AVP-induced pr esser responses were also attenuated with the higher dose of the V-2-recept or antagonist. These findings suggest that AVP tonically enhances barorefle x function through a V-2 receptor in the SHR.