Intranasal Oxytocin has sympathoexcitatory effects on vascular tone in healthy males.

OBJECTIVE Oxytocin appears to be involved in the neuroendocrine regulation of sympathetic blood pressure (BP) homeostasis. In animals, intracerebral administration of oxytocin induces BP-relevant sympathetic activation. In humans, central nervous effects of oxytocin on BP regulation remain unclear. Intranasal administration supposedly delivers oligopeptides like oxytocin directly to the brain. We investigated the effects of intranasal oxytocin on sympathetic vascular baroreflex function in humans using microneurographic techniques. METHODS In a balanced, double-blind cross-over design oxytocin or placebo was administered intranasally to 12 lean healthy males (age 25±4 years). MSNA was assessed microneurographically before (pre), 30-45 (post-I) and 105-120 minutes (post-II) after oxytocin administration. Baroreflex was challenged via graded infusions of vasoactive drugs and correlation of BP with MSNA and heart rate (HR) defined baroreflex function. Experiments were conducted in the afternoon after a 5h fasting period. RESULTS After oxytocin, resting MSNA (burst rate and total activity) showed significant net-increases from pre to post-II compared to placebo (∆-increase: +4.3±1.2 (oxytocin) vs. +2.2±1.4 burst/min (placebo), ANOVA p<0.05; total activity 184±11.5% (oxytocin) vs. 121±14.3% (placebo), ANOVA; p=0.01). This was combined with a small but significant net-increase in resting diastolic BP, while systolic and mean arterial BP or HR as well as baroreflex sensitivity at vasoactive drug challenge were not altered. CONCLUSION Intranasally administered oxytocin induced vasoconstrictory sympathoactivation in healthy male humans. The concomitant increase of diastolic BP was most likely attributable to increased vascular tone. This suggests oxytocin-mediated upward resetting of the vascular baroreflex setpoint at centers superordinate to the mere baroreflex-feedback-loop.