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Furthermore, the combination of the molecular process models (e.g. Miller et al. 2010) with models relating [http://en.wikipedia.org/wiki/GPX4 GPX4] receptor input to adaptive effects on channels (Vadigepalli et al. 2007) indicates a future role for simulation studies that connect molecular processes with neurophysiology. Taking the present approach to the study of specific neurons identified by markers of interest, in the present case A2 cells, radically expands our understanding of these neuron types and of their cell-type-specific adaptive response to the blood pressure disturbance. The identification of specific molecular participants in the adaptive response to blood pressure will predict useful targets to explore using genetic manipulation technologies. We acknowledge the experimental and computational contributions of Monica Payne, Carmen Nichols, PhD, Peter Ucciferro, Albert Babinskas, Alexandria Starks and Gregory M. Miller. We thank Kate Freeman, MD, for her critical reading of the manuscript. This work was financially supported by NIH grants R01 GM083108, R33 HL088283 and R33 HL087361. ""What is the central question of this study? Patients with heart failure often develop ventilatory abnormalities at rest and during exercise, but the mechanisms underlying [http://www.selleckchem.com/products/azd9291.html Osimertinib molecular weight] these abnormalities remain unclear. This study investigated the influence of inhibiting afferent neural feedback from locomotor muscles on the ventilatory response during exercise in heart failure patients. What is the main finding and its importance? Our results suggest that inhibiting afferent feedback from locomotor muscle via intrathecal opioid administration significantly reduces the ventilatory response to exercise in heart failure patients. Patients with heart failure (HF) develop ventilatory abnormalities [http://www.selleckchem.com/products/ch5424802.html Alectinib datasheet] at rest and during exercise, but the mechanism(s) underlying these abnormalities remain unclear. We examined whether the inhibition of afferent neural feedback from locomotor muscles during exercise reduces exercise ventilation in HF patients. In a randomized, placebo-controlled design, nine HF patients (age, 60 �� 2 years; ejection fraction, 27 �� 2%; New York Heart Association class 2 �� 1) and nine control subjects (age, 63 �� 2 years) underwent constant-work submaximal cycling (65% peak power) with intrathecal fentanyl (impairing the cephalad projection of opioid receptor-sensitive afferents) or sham injection. The hypercapnic ventilatory response was measured to determine whether cephalad migration of fentanyl occurred. There were no differences in hypercapnic ventilatory response within or between groups in either condition. Despite a lack of change in ventilation, tidal volume or respiratory rate, HF patients had a mild increase in arterial carbon dioxide () and a decrease in oxygen (; P