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J.J. Bonica Lecture—2000: Physiology, Pathophysiology, and Pharmacology of Visceral Pain
  1. G. F. Gebhart, Ph.D.
  1. From the Department of Pharmacology, College of Medicine, The University of Iowa, Iowa City, Iowa.
  1. Reprint requests: G.F. Gebhart, Ph.D., Department of Pharmacology, University of Iowa College of Medicine, 2-471 BSB, Iowa City, IA 52242-1109. E-mail: gf-gebhart{at}


Background and Objectives The principal objective of this report is to review recent experimental advances in our understanding of the physiology and pathophysiology of visceral pain and to describe results of studies of opioid modulation of visceral nociception.

Methods Results are drawn from electrophysiological studies of single pelvic nerve afferent fibers innervating the descending colon in the rat.

Results The important findings include the following: identification of a subset of pelvic nerve fibers that likely function to signal acute visceral pain, sensitization of mechanosensitive pelvic nerve fibers, and documentation of the presence of silent nociceptors in the pelvic nerve. With respect to pharmacological modulation of pelvic nerve fiber responses to colonic distension, only kappa-opioid receptor agonists, and not mu- or delta-opioid receptor agonists, were effective.

Conclusions All pelvic nerve fibers innervating the descending colon can be sensitized and contribute to visceral pain; their responses are modulated by kappa-opioid receptor agonists acting in the periphery.

  • Kappa opioids
  • Mechanoreceptors
  • Colon distension
  • Afferent fibers
  • Polymodal
  • Antisense

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  • Supported by National Institutes of Health awards NS19912, DA 02879, and NS35790.