Vasopressinergic augmentation of cardiac baroreceptor reflex in conscious rats.

Experiments were performed on conscious, chronically instrumented rats to determine the contribution of V2-receptor activation in augmentation of cardiac baroreceptor reflex (BRR) sensitivity by arginine vasopressin (AVP). At least 1 wk before experimentation, rats were implanted with arterial and venous catheters, as well as with pulsed Doppler flow probes for measurement of cardiac output (CO). An initial set of experiments was performed to determine whether cardiac BRR sensitivity is enhanced by AVP in conscious rats. A series of pressor doses of either AVP or phenylephrine (PE) were administered on separate days (n = 8). The slope of pulse interval (PI) vs. mean arterial blood pressure (MABP) was determined for each experiment by linear regression and used as an index of cardiac BRR sensitivity. The slope of PI vs. MABP was greater in response to AVP than in response to PE in all animals studied. A separate group of animals (n = 7) received either a 40-min infusion of AVP (5 ng/min iv) or a specific V2-antagonist, d(CH2)5[DIle2,Ile4]AVP (20 micrograms/kg iv), 10 min before infusion of AVP. The responses of MABP, CO, and total peripheral resistance to AVP infusion were similar with and without V2-antagonism; however, the bradycardic response to AVP was less with V2-antagonist pretreatment. Furthermore, administration of V2-antagonist reduced delta PI/delta MABP in response to AVP infusion. Additional experiments were performed to test the effect of infusion of a specific V2-agonist, dVDAVP (5 ng/kg iv), on BRR-induced bradycardia in response to a series of pressor PE bolus doses.(ABSTRACT TRUNCATED AT 250 WORDS)