In a rat model, BDNF was identified as a candidate molecule for the mediator of activity-dependent changes at baroafferent synapses during hypertension [11], while it has also been shown to quickly alter the neurotransmitter release properties of sympathetic neuron-myocyte connections in rodent cell cultures, leading to a rapid shift from excitatory to inhibitory cholinergic transmission in response to neuronal stimulation [35]. This evidence concerns the gene BDNF and hypertensive disorder.