AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 6 1429-R1435, Copyright © 1989 by American Physiological Society
Synthetic capsaicin reversibly impairs vasopressin-mediated blood pressure recovery
S. M. Gardiner, T. Bennett and T. P. O'Neill
Department of Physiology and Pharmacology, Queen's Medical Center, Nottingham, United Kingdom.
The vasopressin-mediated recovery of arterial pressure observed in adult
rats following pharmacological blockade of the sympathetic nervous and
renin-angiotensin systems is reduced by neonatal capsaicin treatment. We
now demonstrate a similar but reversible effect following treatment of
adult Wistar or Sprague-Dawley rats with N-vanillylnonanamide (50 mg/kg
sc). One day after treatment, Wistar, but typically not Sprague-Dawley,
rats had lost weight and exhibited increased sensitivity to the anesthetic
effects of methohexital sodium. In both strains, captopril treatment caused
hypotension. After captopril and ganglionic blockade, vasopressin-mediated
recovery of arterial pressure was significantly inhibited. Furthermore,
treated Wistar rats had reduced sensitivity to the ocular irritancy of
N-vanillylnonanamide when examined 2 days postdose. All deficits reversed
within 2 wk of dosing. These data suggest that capsaicin-sensitive systems
participate in homeostatic mechanisms engaged during acute hypotension.
Because the dose of N-vanillylnonanamide employed in the present study has
previously been shown to destroy unmyelinated afferent fibers when
administered to adult rats, recovery of the functional deficits may reflect
regeneration of damaged processes or assumption of their function by
undamaged neurons innervating adjacent sites. By extrapolation from other
studies of capsaicin, damage to some central neurons may also be involved.
