Paraventricular nucleus corticotropin-releasing hormone (CRH) neurons are activated by neural inputs from a number of possible sources (Figure 1). Stressors signaling homeostatic challenge (commonly referred to as systemic stressors) are mediated by neurocircuits providing direct excitation of paraventricular nucleus (PVN) neurons. For example, HPA-axis activation by blood loss (hemorrhage) is mediated by activation of brainstem norepinephrine neurons that project directly to the PVN. Activation of the HPA axis by fluid imbalance appears to be triggered by angiotensinergic neurons of the subfornical organ, which sense increases in circulating angiotensin II. Negative energy balance signals are relayed to the PVN by the arcuate nucleus, which activates CRH neurons by release of excitatory peptide messengers (such as neuropeptide Y and agouti-related peptide). Responses to systemic stress are thought to be reflexive, that is, they do not require the engagement of cognitive processes.
The heart has an intrinsic conduction system that causes electrical activity in the heart muscles causing them to contract. The intrinsic conduction system is made up specialized cells, that contain nerve and muscular characteristics.
The muscle cells in the heart are linked together by gap junctions, allowing cardiac action potentials to travel from one muscle cell to another.
Atrioventricular (AV) node. The damage to the AV node causes the electrical signals traveling from the upper chambers to the lower chambers to be impaired causing an AV block.
