The parabrachial nucleus mediates the decreased cardiac baroreflex sensitivity observed following short-term visceral afferent activation.

Previous investigations have provided evidence demonstrating that the extracellular release of glutamate into the parabrachial nucleus was significantly enhanced following visceral afferent activation. This period of enhanced glutamate release into the parabrachial nucleus corresponded to a time during which the pressor response to a bolus phenylephrine injection was significantly enhanced, and the reflex bradycardia was attenuated. This decrease in the sensitivity of the baroreflex is suggestive of an enhanced sympathetic tone as a result of the vagal stimulation. The present investigation was done to determine if the decreased baroreflex sensitivity observed following short-term vagal stimulation is mediated by an increase in sympathetic activity and was dependent on the parabrachial synapse. Male Sprague-Dawley rats were anaesthetized with sodium thiobutabarbitol and instrumented to monitor blood pressure and heart rate and for the placement of a stimulating electrode on the left cervical vagus nerve. Femoral arterial blood samples were taken before, during and after 2 h of vagal stimulation which were later assayed for plasma catecholamines. The results showed that plasma norepinephrine levels decreased during, and were significantly elevated immediately following termination of the vagal stimulation, indicative of an increase in sympathetic tone. To determine if the parabrachial nucleus is involved in mediating an enhanced sympathetic activity following vagal stimulation, a second group of animals underwent an identical surgical preparation, vagal stimulation and blood sampling protocol with the addition of bilateral microinjections of either the reversible anaesthetic, lidocaine, or saline into the parabrachial nucleus. The results showed that reversible blockade of the parabrachial nucleus prior to the onset of the vagal stimulation was effective in blocking both the elevation in plasma norepinephrine levels and the depressed baroreflex sensitivity previously observed following 2 h of vagal stimulation. These results suggest that the parabrachial nucleus mediated the sympathoexcitation and consequent depression in baroreflex sensitivity observed following visceral afferent activation.