This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator.
The specific aim i s to determine is ischemic metabolites acutely sensitize muscle mechanoreflex control or RCVR. We hypothesize that in normal humans, ischemic metabolites, such as prostaglandins, acutely sensitize muscle mechanoreceptors during exercise resulting in augmented mechanoreceptor control of muscle sympathetic nerve activity (MSNA) and renal cortical vascular resistance (RCVR), and that this augmented mechanoreceptor control is exaggerated in patients with HF.
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