Chemoreflex Function in Heart Failure Continued

Harold Schultz and Shu-Yu Sun Central chemoreceptors, located on the central surface of the medulla, have also been found to play a role in increased activation of sympathetic activation of the chemoreflex. However, there are alternative methods suspected to lead to increased central chemoreceptor sensitivity. This main mechanisms being angiotensin two regulation mediating the alteration of baro and chemoreceptor sensitivity. Two key pieces of evidence lead to this hypothesis 1) angiotensin two levels are elevated in chronic heart failure patients and 2) Angiotensin two in the central nervous system can stimulate sympathetic ouflow, blunt baroreflexes, and stimulate breathing. It was seen that the administration of angiotensin two inhibitors in HF rabits reversed the enhanced peripheral chemoreflex function and improved baroreflex function. Ironically, the treatment they authors suggest to improve hemodynamic profiles as well as ventilatory response, decreasing the sympathetic activation in HF patients is exercise. I find this ironic because in most cases exercise will prevent HF in the first place. The reason that the authors believe exercise helps in decreasing sympathetic activation is because it increases NO synthesis which is thought to help regulate peripheral chemoreflex sensitivity. ~JI