Abstract

In rats, arginine vasopressin augments bradycardia associated with baroreflex activation. We investigated whether modulation of peripheral cardiac parasympathetic nerve function by AVP may play a role in this effect. To accomplish this we utilized an in vivo model with which we previously demonstrated both adrenergic and peptidergic modulation of cardiac parasympathetic nerve function. Urethane-anesthetized rats (250-350 g) were prepared with arterial and venous catheters and ECG leads. The cervical vagi were sectioned, and propranolol (1 mg/kg, i.v.) was administered to eliminate reflex changes in heart rate. To investigate potential preganglionic modulation by AVP, the right vagus nerve was electrically stimulated (0.5 mA; 0.5 msec; 1-10 Hz). To observe postganglionic effects through nicotinic activation, carbachol (a mixed nicotinic and muscarinic agonist) was injected (0.5 to 4.0 micrograms/kg, i.v.). To observe direct cholinergic effects at the SA node, methacholine (a pure muscarinic agonist) was injected (0.5 to 4.0 micrograms/kg). All three trials were performed before (control) and during AVP infusion (20 micrograms.kg.min). No consistent, significant differences in vagal-, carbachol- or methacholine-induced bradycardia were observed between control and AVP groups. Since endogenous plasma levels of AVP in the control situation may have saturated any vasopressinergic effect prior to AVP infusion, the experiments were repeated in Brattleboro rats, genetically deficient in AVP. Again, no consistent differences in heart rate responses to parasympathetic activation were noted between control and AVP-infused groups. These results suggest that in rats, vasopressinergic augmentation of baroreflex-induced bradycardia is not mediated by an effect on the peripheral cardiac parasympathetic innervation. However, it remains to be investigated whether AVP-mediated sympathetic withdrawal disinhibits cardiac parasympathetic nerve function.

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