CGRP-rich nerve fibers are components of the primary afferent nervous system, comprising principally capsaicin-sensitive C- and A8-fiber nerves that respond to chemical, thermal, and mechanical stimuli (2,10,13). Although these nerves have traditionally been thought to "sense" stimuli in the periphery and transmit the information centrally, there was early evidence that they also have an efferent function. It is clear that DRG neuron-derived peptides are released at peripheral sensory nerve terminals in the absence of afferent nerve stimulation (13). The continuous release of peptides from DRG neurons may reflect a paracrine function implying that these neurons participate in the continuous regulation of blood flows and other tissue activities. Indeed, it has been postulated that some DRG neurons are specialized in controlling peripheral effector mechanisms, but have no role in sensation (13). Sensory nerve terminals can release CGRP in response to local factors including nerve growth factor (NGF) (10,14), vascular wall tension (10,13), bradykinin/prostaglandins (15,16), endothelin, and the sympathetic nervous system (17). Our laboratory has demonstrated that these same factors that alter the acute release of CGRP can also modulate the long-term production and release of this peptide. Using primary cultures of adult rat DRG neurons, we have reported that NGF or bradykinin/prostaglandins (15,16) can stimulate CGRP synthesis and release, whereas glucocorticoids (18) or «2-adrenoreceptor agonists (14) inhibit the stimulatory effects of NGF on CGRP. Thus, alterations in these factors, some of which are known to occur in hypertension, may mediate any changes seen in CGRP expression.
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