Receptor-mediated stimulation and inhibition of nerve growth factor secretion by vascular smooth muscle

Nerve growth factor (NGF) is a potent neurotrophin signaling protein, the best-known member of a family of similar neurotrophins. Specific neuronal populations depend upon the neurotrophins for normal function and disturbances in NGF and neurotrophin supply have been implicated in neurodegenerative disease, diabetes, and hypertension. This report details experiments in which the hourly pattern of NGF secretion by cultured vascular smooth muscle cells is examined. Vascular smooth muscle cells are major innervation targets of the neuronal population first discovered to be NGF-dependent: the sympathetic principal neurons. The results show that arginine vasopressin (AVP), angiotensin II (AngH), and α-adrenergic receptor activation, all contractile stimuli, elevate NGF secretion. However, AVP dependably does so alone while AngH requires coactivation of adenosine receptors. Adenosine alone inhibits secretion mid the α-adrenergic increase in NGF output can be antagonized by activation of β-adrenergic receptors. A change to fresh culture medium is also a potent stimulus to increased NGF output.