AJP - Gastrointestinal and Liver Physiology, Vol 263, Issue 1 29-G37, Copyright © 1992 by American Physiological Society
Peptidergic nerves mediate post-nerve stimulation hyperemia in rat gut
O. D. Hottenstein, G. Remak and E. D. Jacobson
Department of Physiology, University of Colorado Health Sciences Center, Denver 80262.
Cessation of perivascular nerve stimulation (NS) elicits a transient
increase in intestinal blood flow above the prestimulatory value. This
enhancement of blood flow constitutes the phenomenon of post-nerve
stimulation hyperemia (PSH). We investigated the involvement of peptidergic
sensory nerves in intestinal PSH. In anesthetized rats the velocity of
blood flowing through the anterior mesenteric artery (VBF) was measured
with a pulsed Doppler velocimeter. PSH was induced by 4 min of
postganglionic electrical NS (5 Hz). PSH was abolished by distal
periarterial application of tetrodotoxin and intra-arterial lidocaine,
which suggests a peripheral sensory nervous mechanism for PSH. The increase
in conductance at peak PSH was blocked by pretreatment with the selective,
primary afferent neurotoxin capsaicin administered as 1) subcutaneous
injection in neonatal life, 2) topical application to periarterial nerves,
or 3) injection into the jejunal lumen. In rats pretreated with reserpine,
NS evoked a hyperemic response, which was blocked by capsaicin. Treatment
with adenosine deaminase inhibited PSH considerably less than capsaicin,
suggesting a lesser role for adenosine in PSH. Our findings support the
hypothesis that postganglionic NS activates both adrenergic and peptidergic
nerves and that the latter release vasodilator peptides in the gut during
PSH.
