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Division of Cardiovascular Medicine, Departments of Internal Medicine and Human Physiology, University of California, Davis, California 95616
Abdominal ischemia reflexly activates
the cardiovascular system by stimulating abdominal visceral afferent
nerve endings. Whereas many ischemic metabolites responsible for
activating these nerves have been identified (e.g., bradykinin), their
precise mechanism of action is unclear. Protein kinase C (PKC) is an
important part of the signal transduction process underlying the action of metabolites such as bradykinin and is a regulator of neuronal activity. Therefore, we hypothesized that PKC contributes to
stimulation of ischemically sensitive abdominal visceral afferents.
Single-unit activity was recorded from the right thoracic sympathetic
chain of anesthetized cats. Exogenous activation of PKC using phorbol 12,13-dibutyrate (PDBu, 5 µg/kg ia) increased the impulse activity of
ischemically sensitve C-fiber afferents from 0.04 ± 0.01 to 0.67 ± 0.23 impulses/s (n = 11;
P < 0.05). The influence
of endogenous activation of PKC also was evaluated during 10 min of
mesenteric ischemia. Inhibition of PKC using PKC-(19
36) (20 µg/kg iv) reduced ischemia-induced increases in afferent
activity from 0.46 ± 0.11 to 0.19 ± 0.08 impulses/s
(n = 7, P < 0.05). Moreover, PKC-(1936) (20 µg/kg iv) reduced the response of ischemically sensitive C fibers
to bradykinin (0.5-1.0 µg/kg ia) from 1.18 ± 0.20 to 0.66 ± 0.14 impulses/s (n = 13, P < 0.05). These results indicate
that PKC contributes to activation of abdominal visceral afferents during ischemia and specifically to part of the
bradykinin-induced activation of these afferents.
abdominal ischemia; sympathetic afferents; nociception; phorbol ester; cat
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