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Subsequently, the drug molecule can undergo further substitution with additional lipophilic groups at sites distant from that are involved in receptor binding [46]
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In reverse mode NET causes an efflux of the cytoplasmic pool of presynaptic norepinephrine into the synaptic cleft, where it can activate postsynaptic α-1 and β-1 receptors to elevate systemic vascular resistance and stimulate cardiac output (Vansal & Feller 1999
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