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. 2015 Feb 11;308(8):H792–H802. doi: 10.1152/ajpheart.00830.2014

Fig. 3.

Fig. 3.

Mechanisms by which a myocardial infarction, or similar injury, provokes sympathetic excitation. Lowered cardiac output decreases the arterial baroreflex inhibition on efferent MSNA, which provokes peripheral vasoconstriction. The chronic renal hypoperfusion leads to activation of the renin angiotensin system and generates skeletal muscle inflammation and atrophy. The result of these alterations is skeletal myopathy. Abnormal chemoreflex activity and abnormal skeletal muscle reflex control lead to increased ventilation. NO, nitric oxide; RSNA, renal sympathetic nerve activity.