Activation of cardiac vagal afferents facilitates late vagal inhibition in neurones of the rostral ventrolateral medulla oblongata bilaterally.

A reduced activity of cardiac vagal afferent fibres is considered as one of the pathophysiological causes of post-infarction complications [A. Head, Baroreflexes and cardiovascular regulation in hypertension. J. Cardiovasc. Pharmacol. 26 (1995) S7-S16]. The mechanism of how a reduction of cardiac vagal activity leads to enhanced sympathetic drive and systemic hypertension is however not yet clear. Experimental data have shown that the rostral ventrolateral medulla oblongata (RVLM) plays an important role in tonic blood pressure regulation, the control of sympathetic vasoconstriction and cardiac performance. The aim of the study was to determine whether activation of cardiac vagal afferents contributes to eliciting the long-lasting late inhibition that we have previously shown to occur in neurones of the RVLM [A. Zagon, K. Ishizuka, I. Rocha, K.M. Spyer, Late vagal inhibition in neurones of the ventrolateral medulla oblongata in the rat. Neurosci. 92 (1999) 877-888]. The experiments were carried out in terminally anaesthetised and artificially ventilated rats using in vivo intracellular recordings. The data confirmed that late vagal inhibition is elicited by cumulative activation of functionally different vagal afferents, including those that originate from cardiac receptors. It was also demonstrated that activation of cardiac afferents could lead to a significant increase in the duration of this long-lasting late response component. Facilitation of late vagal inhibition was observed in RVLM neurones both ipsi- and contralateral to the stimulated nerve. It is suggested that such facilitation of late vagal inhibition may be a mechanism of how pulse-synchronous activation of cardiac afferents leads to a tonic modulation of the activity of RVLM neurones. An attenuation of late vagal inhibition during reduced activity of cardiac vagal afferents could lead to enhanced excitability in these neurones which in turn can lead to an increase in medullary sympathetic outflows towards the heart and peripheral blood vessels.