The baroreflex regulates cardiovascular dynamics by integrating afferent feedback signals from the heart and blood vessels with parasympathetic (PNS) and sympathetic (SNS) efferent activity to cardiovascular end organs. In addition to known brainstem pathways there is growing evidence from neuroanatomical, clinical and surgical neurostimulation studies that forebrain cortical sites have an important role in modulating cardiac rhythms and blood pressure through the autonomic nervous system (Cechetto & Saper, 1990; Critchley et al. 2003; Oppenheimer et al. 1992). These sites include the insular cortices (IC), anterior cingulate cortex (ACC), medial prefrontal (mPFC), amygdala and cerebellum. Recent advances in neuroimaging technologies have allowed exploration of this cortical autonomic network (CAN) in conscious humans. Studies using effortful volitional and cognitive tasks have associated activity in the dorsal ACC and IC regions with autonomic aspects of cardiovascular arousal. However, such tasks produce elevations in heart rate (HR) and mean arterial pressure (MAP) as well as changes in PNS and SNS efferent activity. As afferent signals from the heart and baroreceptive vascular regions are represented in the forebrain, and efferent signals generate changes in HR and MAP, it remains uncertain whether the cortical activity during volitional effort represents viscerosensory or visceromotor components of baroreflex-mediated cardiovascular arousal and/or muscle activation. Our goal has been to study the cortical organization of baroreflex-cardiovascular integration and differentiate the afferent and efferent components. Functional magnetic resonance imaging (fMRI) is used to assess cortical activation patterns during various manoeuvres that differentially affect HR, MAP, sympathetic nerve activity (SNA) and cardiac output. Our findings presented here focus on the most robust responses in the CAN. During a 30-sec isometric handgrip (IHG) contraction of moderate intensity (e.g. 30% maximal), both HR and MAP are increased (Wong et al. 2007b; Wong et al. 2007a). The tachycardia is due to PNS withdrawal and is associated with deactivation in the mPFC and bilateral IC activation. Additional studies were designed to differentiate the baroreceptor “loading” phase from concurrent bottom-up changes in MAP and HR from top-down volitional effort during IHG. HR rises rapidly during a 2-sec isometric contraction whereas the MAP response is delayed, cresting 2-5 sec after the contraction. During a 30% maximal effort IHG lasting 2-sec, where HR increases but SNA is unchanged, deactivation in vMPFC is observed along with bilateral IC activation. SNA does increase during a strong (e.g. 70% maximal) 2-sec contraction, along with HR, and is associated with additional activation in the dACC. However, the post-contraction rise in MAP was associated with activation only in the left posterior IC. More direct and physiologic assessment of baroreflex control can be accomplished using low to moderate levels of lower body negative pressure (LBNP) that unloads the baroreceptors through reductions in central filling pressure and pulse pressure. In this model MAP remains constant and the HR and SNA responses can be differentiated with varying levels of suction. When only SNA rises (-15 mmHg suction) dACC and/or genual ACC activation is observed along with right posterior superior IC activation. When both HR and SNA rise (-35 mmHg), additional deactivation in the mPFC, amygdala, and bilateral central IC (emphasizing posterior inferior right IC) is observed (Kimmerly et al. 2005; Kimmerly et al. 2007a; Kimmerly et al. 2007b). Passive rises in MAP and reductions in HR were elicited with phenylephrine infusions producing a direct arterial baroreflex effect. These events are associated with mPFC activation (i.e. mPFC is still negatively correlated with HR), bilateral inferior IC activation and dACC activation. In summary, the studies suggest that: 1) baroreceptor loading through increased MAP (passive and active) produces bilateral (and predominantly left) anterior IC activation; this suggests a viscerosensory role of these regions. 2) During baroreceptor unloading with stable MAP (LBNP), increased SNA alone is associated with right superior posterior IC activation; if both SNA and HR increase there is additional activation in the dACC and deactivation in the mPFC and inferior IC regions. 3) Changes in SNA, be they an increase or decrease, were always associated with activation of the dACC or genual ACC. 4) Changes in HR were always negatively correlated with mPFC. Our studies emphasize the CAN regions that are involved in reflex cardiovascular control, independent of effort.