Oxytocin in the NTS

Abstract

The role of brain stem oxytocinergic projections in the modulation of heart rate control during exercise is discussed on the basis of both changes in endogenous peptide content and heart rate changes observed during exercise. Running on a treadmill caused an increase in oxytocin content in dorsal/ventral brain stem areas and spinal cord, specifically in trained rats. Trained rats pretreated with a specific oxytocin receptor antagonist into the dorsal brain stem area (corresponding to the nucleus tractus solitarii and dorsal motor nucleus of the vagus, or NTS/DMV) showed a significant potentiation of exercise tachycardia with no change in the blood pressure response. The same treatment in sedentary rats was without effect. On the other hand, administration of exogenous oxytocin into this area caused significant blunting of exercise tachycardia in both groups, with no change in the pressure response. It is proposed that long-descending oxytocinergic pathways from the hypothalamus to the NTS/DMV area serve as a link between the two main neural controllers of the circulation--that is, the central command and feedback control mechanisms driven by the peripheral receptor signals. Our results strongly suggest that oxytocinergic input to NTS/DMV, by restraining the tachycardic response of trained individuals, contributes to the smaller response observed after training, without compromising cardiac output adjustment and the circulatory demand during exercise.