Vasopressin facilitates inhibition of renal nerve activity mediated through vagal afferents

We measured the effect of vasopressin (8 mU·kg^-1·min^-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 ± 0.7 to 14.1 ± 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 ± 6.9 to 30.2 ± 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 ± 1.0 to 7.3 ± 1.1 mmHg and decreased RNA from 61.8 ± 7.2 to 47.1 ± 6.3 impulses/s. Heart rate fell from 243 ± 7 to 231 ± 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 ± 1.2 mmHg and decreased RNA to 17.0 ± 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 ± 1.1%/mmHg before vasopressin and nearly doubled (-11.9 ± 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.